Introduction
Babesiosis is caused by any one of many Babesia species
that infect a wide variety of vertebrate hosts, including domestic and wild animals, as
well as man. In nature, babesias typically are transmitted biologically by ixodid ticks,
but other means, such as biting flies and fomites that transfer blood from the infected
carrier to a susceptible animal, may be involved in the mechanical transmission of these
intraerythrocytic parasites. A list of commonly encountered babesias is presented in table
1. Although it is possible for a single Babesia species to infect more than one
vertebrate host, as seen in B. microti (rodents and man) and B. divergens (cattle, man, and gerbils), the general pattern is that the Babesia species are
reasonably host specific.
This review will deal primarily with those babesias afflicting
cattle. It is thought that these animals are, from an economic point of view, the most
severely affected by babesial infections. Equine babesiosis and babesiosis of other
animals are discussed briefly in this chapter.
Bovine Babesiosis
(Piroplasmosis, Texas fever, redwater, tick fever)
Definition
Bovine babesiosis is a febrile, tick-borne disease of cattle,
caused by one or more protozoan parasites of the genus Babesia and generally
characterized by extensive erythrocytic lysis leading to anemia, icterus,
hemoglobinuria,and death.
There are probably at least six Babesia species (Table 1) responsible for bovine babesiosis. Most can be categorized as
being small or large babesia. Morphological and serological differences are used to
distinguish the different species. The two that are of most concern in the United States
are B. bigemina and B. bovis, which are transmitted primarily by Boophilus ticks. These species and their vector ticks once occurred in large areas of the United
States, and still occur in Mexico and throughout the tropical and subtropical areas of the
Western Hemisphere.
"Babesia bigemina"
Etiology
B. bigemina (Fig. 29) is a large babesia that is pleomorphic but
characteristically is seen and identified by the pear-shaped bodies joined at an acute
angle within the mature erythrocyte. Round forms measure 2 µm and the pear-shaped,
elongated ones are 4-5 µm (1).
History
One of the early accounts in the United States of babesiosis dates
from 1868, when a disastrous epizootic broke out among native cattle in Illinois and
Indiana with the loss of 15,000 head after the importation of apparently healthy cattle
from Texas (2). The mortality rate among affected cattle approached 90 percent. The fear
and respect for Texas or southern cattle fever was wellfounded. Even then it was not a new
disease, having been described as early as 1814. It was not, however, until much later
that the cause and mode of transmission became apparent.
The classical investigations of Smith and Kilborne (1893) were the
first to establish that a pathogenic protozoan (B. bigemina) could be transmitted
by an intermediate arthropod host (Boophilus annulatus) (3). At that time, Boophilus ticks, and presumably babesiosis, occurred in the United States throughout the South, from
Texas to the Atlantic States, as well as in southern California (Illustration 1) (4). In
1906, it was estimated that economic losses associated with the tick, and B. bigemina (probably B. bovis also) amounted to $130.5 million annually. In terms of present
dollars, and considering the larger number of cattle now present in the South, these
losses would easily exceed a billion dollars annually if ticks and babesias were left
uncontrolled. A tick eradication program was essentially completed by 1943, and bovine
babesiosis ceased to exist in the United States except in the quarantine buffer zone
adjacent to the Mexican border (4). Babesiosis is now considered an exotic disease of
cattle for the United States. This impressive accomplishment of tick eradication has never
been duplicated in an area of comparable size, notwithstanding similar efforts in various
parts of the world. As a result of those failures, both ticks and babesia are widely
prevalent elsewhere and constitute a continuing threat to U.S. livestock.
Host Range
Cattle are the principal hosts, but it is reported that the water
buffalo and African buffalo may also become infected (11). It is possible that other
ungulates are infected, but from a practical point of view, these infections are nominal
and, except under unusual conditions, rare. Such hosts are probably not significant
reservoirs of infection.
Babesia bigemina is widespread in cattle and occurs
wherever Boophilus ticks are encountered, which includes North and South America,
Southern Europe, Africa, Asia, and Australia (10). Babesiosis also occurs on the Caribbean
and South Pacific islands. Cattle and the invertebrate tick hosts provide the major
reservoir of infection. Wildlife and nonbovine hosts generally have not been incriminated.
Transmission
Ticks acquire babesia infection during their feeding on infected
animals. The infection is then passed to the ovaries, and thus the emerging larvae carry
the infection. The babesias continue to develop within the larvae, and transmission
usually occurs in the new host during the nymphal and adult stages. Boophilus annulatus, B. microplus, and B. decoloratus are the principal vectors of B. bigemina (5,6). Mechanical transmission is possible, but it is not efficient enough to maintain
infection in the absence of specific tick vectors.
Incubation Period
Natural transmission occurs by the feeding of infected nymphal and
adult ticks, and evidence of infection occurs 2-3 weeks after tick infestation. Following
blood inoculation, the incubation time may be 4-5 days or less, depending on the size of
the exposing inoculum.
Clinical Signs
Infection with B. bigemina is usually accompanied by the
presence of Boophilus ticks. Calves normally are reasonably resistant to babesia,
for the infection does not usually result in clinical disease (5). In older animals,
clinical signs can be very severe; however, differences in pathogenicity may occur with
various B. bigemina isolates associated with different geographic areas.
Mahoney observed that the Australian B. bigemina rarely causes disease, whereas B.
bigemina in Africa is highly pathogenic (6). Personal experience by the author
suggests that B. bigemina as seen in the Western Hemisphere is highly pathogenic;
however, it is probably less so than B. bovis.
The first sign is usually a high fever with rectal temperatures
reaching 41.5o C (106.7o F). There is anorexia, and ruminal atony.
Often the first visible appearance of infection is that the animal isolates itself from
the herd, becomes uneasy, seeks shade, and may lie down. Cattle may stand with an arched
back, have a roughened hair coat, and show evidence of dyspnea and tachycardia. The mucous
membranes are first injected and reddened, but as erythrocytic lysis occurs, the color
changes to the pallor of anemia. Anemia is a contributory factor to the weakness and loss
of condition seen in cattle that survive the acute phase of the disease. The anemia may
occur very rapidly, with 75 percent or more of the erythrocytes being destroyed in just a
few days. This is usually associated with severe hemoglobinemia and hemoglobinuria. After
onset of fever, the crisis will usually pass within a week, and if the animal survives,
there is usually severe weight loss, drop in milk production, possible abortion, and a
protracted recovery. Mortality is extremely variable and may reach 50 percent or higher,
but in the absence of undue stress most animals will survive (5,6).
Gross Lesions
The lungs may be edematous and congested in cattle that have died
early in the course of infection. The pericardial sac may contain serosanguineous fluid
and subepicardial and subendocardial petechial hemorrhages. The liver is enlarged and
icteric, and the gallbladder, which may have hemorrhage on the mucous surface, is
distended with thick, dark green bile. The spleen is markedly enlarged, and has a dark
pulpy consistency. The abomasal and intestinal mucosa may be icteric with patches of
subserosal hemorrhages. The blood is thin and watery. The urinary bladder is frequently
distended, with dark, reddish-brown urine. Jaundice is commonly distributed in the
connective tissue. The lymph nodes are edematous and often have petechiation.
In cattle that have suffered a more prolonged illness, acute
lesions are much less conspicuous. Subepicardial petechial hemorrhages may be present, the
carcass is usually emaciated and icteric, the blood is thin and watery, the intermuscular
fascia is edematous, the liver yellowish-brown, and the bile may contain flakes of
semisolid material. The kidneys are pale and often edematous, and the bladder may contain
normal urine, depending on how long past the hemolytic crisis the necropsy is performed.
Although the spleen is enlarged, the pulp is firmer than in acute babesiosis (5,6,7).
Diagnosis
Field Diagnosis
Fever, anemia, jaundice, and hemoglobinuria are suggestive
clinical signs of babesiosis in cattle located in enzootic areas where Boophilus ticks occur. If these signs are also associated with erythrocytic destruction, the
diagnosis of babesiosis is strengthened. A positive diagnosis requires the identification
of the babesia on blood smears or either positive serologic tests or transmission
experiments, or both.
Specimens for the Laboratory
From each animal six blood smears should be made, air-dried and
fixed in methanol and/or a sample of whole blood in an anticoagulant and serum should be
collected.
In acute infection, B. bigemina can usually be detected on
Giemsa-stained thin blood smears. Thick smears (8) increase the likelihood of detecting
the causative organism, but the characteristic morphology is more difficult to identify
with this technique. In cases of chronic infection, diagnosis is usually made using a
variety of serologic tests for the detection of specific antibodies, since the organism
disappears or is present in extremely low numbers soon after the acute infection.
Differential Diagnosis
Other conditions that should be considered and may resemble
babesiosis are anaplasmosis, trypanosomiasis, theileriosis, leptospirosis, bacillary
hemoglobinuria, hemobartonellosis, and eperythrozoonosis.
Prognosis
After the onset of hemoglobinuria, the prognosis is guarded. Among
fully susceptible older cattle, the mortality may reach 50 percent without treatment.
Among cattle raised in an area where babesiosis is endemic, few, if any, losses occur even
though infection takes place (6). This phenomenon usually reflects early exposure of the
neonates, when they are more resistant, resulting in varying levels of protection. Once
having the infection, the bovine experiences a high level of resistance to reexposure.
Treatment
Successful treatment of B. bigemina depends on early
diagnosis and the prompt administration of effective drugs. There is less likelihood of
success if treatment is delayed until the animal has been weakened by fever and anemia. If
medication is administered early, however, success is the rule, for there are several
effective compounds (Table 2) (14).
One of the first successful treatments was trypan blue. This
treatment may be used to determine the type of infection present. B. bigemina is
susceptible to trypan blue treatment, whereas B. bovis, is not. Generally, the
small babesias are more resistant to chemotherapy. The most commonly used compounds for
the treatment of babesiosis are diminazene diaceturate (3-5 mg/kg), imidocarb (1-3 mg/kg),
and amicarbalide (5-10 mg/kg); however, the quinuronium and acridine derivatives are also
effective (Table 2). Treatment of B. bigemina is so effective in
some instances that radical cures occur that will eventually leave the animal susceptible
to reinfection. For this reason, reduced drug levels are sometimes indicated. Imidocarb
has been successfully used as a chemoprophylactic, that will prevent clinical infection
for as long as 2 months but allow mild subclinical infection to occur as the drug level
wanes, resulting in premunition and immunity (15,16). The relative efficacy of some the
more common compounds used is shown in Table 3.
Vaccination
The most common form of immunization against B. bigemina entails inoculating live organism (attenuated or virulent) into susceptible young cattle
followed by chemotherapy, as needed, to modify the clinical effects; thus, coinfectious
immunity or a state of premunition is induced (6). If older animals are to be so
vaccinated, care may be necessary to prevent serious reactions (17,18). An attenuated
organism has successfully been used in Australia (19). Such a premunition approach,
although useful in endemic areas, would be less desirable in areas where the infection
rate is low because this approach, in essence, establishes a large reservoir of infection.
Experimental trials with nonviable vaccines have been successfully
conducted, but no commercial vaccine of this type is available at this time (6,9). After
having recovered from a premunizing parasitemia cattle will have a degree of sterile
immunity for a short time (20). Carrier infections, if accompanied by reexposure, as is
common in endemic areas, will result in immunity that may persist for the lifetime of the
animal (18). There are instances when antigen variations may occur that might challenge
the immunity of a vaccinated animal. Usually, however, when animals are premunized, even
variants will not produce a clinically detectable reaction (6,9).
Control and Eradication
Preventive Measures
The oldest and probably the most effective procedure for the
control of babesiosis is to control and eradicate its vector, the Boophilus tick
(4). The eradication campaign in the United States conducted in the 1920's and 1930's
relied largely on dipping all cattle every 2-3 weeks in vats charged with arsenical
acaricides (4). These acaricides have been replaced by a wide variety of improved
compounds, including the chlorinated hydrocarbons, carbamates, organophosphates, and
natural and synthetic pyrethrins (4). In some tropical countries, tick control rather than
eradication is the goal. This approach attempts to establish an equilibrium in which the
tick numbers are sufficient to maintain low-level infection in the cattle and hence
immunity to acute babesiosis. Care must be taken, however, to prevent the development of
excessive ticks that could be responsible for livestock losses (12,13). In the absence of
reinfection, the babesias gradually disappear, and the cattle become susceptible; hence, a
desire exists to sustain low levels of exposure to maintain immunizing infections. Tick
control in some areas has been complicated by the development of tick resistance to many
of the common acaricides (4).
Sanitation and Disinfection
Aside from efforts involved in the control and elimination of the
tick vector, sanitation and disinfection do not contribute to an abatement of the disease
incidence in enzootic areas. As with most blood diseases, however, care is recommended in
routine surgery (dehorning, castration, etc.) and needle vaccination procedures to prevent
the accidental transfer of blood from one animal to another, thereby transmitting
infection.
"Babesia bovis"
Etiology
Babesia bovis (Fig. 30) is a small pleomorphic babesia typically identified as a
single body, as small round bodies, or as paired, pear-shaped bodies joined at an obtuse
angle within the mature erythrocyte. The round forms measure 1-1.5 µm, and the
pear-shaped bodies 1.5 by 2.4 µm in size (5,6).
History
Soon after Smith and Kilborne's work, the presence of a second
morphologically distinct small babesia of cattle occurring in Argentina was identified as B.
argentina. This was later determined to be synonymous with B. bovis (21). Rees
in 1930 described a small babesia in Louisiana that he determined to be B. bovis (21). If one studies the early drawings of Smith and Kilborne, it is evident that both B.
bigemina and B. bovis were present even then. The history of this organism
closely follows that of B. bigemina, and it is sometimes difficult to distinguish
one from the other in the early literature.
Host Range
Although cattle are the principal hosts, it is probable that
infections can be maintained in other ungulates such as buffalo (11). There are reports in
the literature of human cases due to B. bovis (24).
Geographic Distribution
Babesia bovis usually occurs in the same areas a B.
bigemina and in association with Boophilus ticks but has been described in some
parts of Europe where Boophilus does not occur, which suggests other vectors.
Transmission
The same ticks (B. annulatus, B. microplus) that
transmit B. bigemina are usually capable of transmitting B. bovis. The tick B.
decoloratus, which is widely distributed in Africa, does not appear to transmit B.
bovis even though it readily transmits B. bigemina (9). There are reports from
Europe of B. bovis, for which the vector is thought to be Ixodes ricinus (11,23).
Incubation Period
B. bovis has a longer incubation time than does B.
bigemina, but since B. bovis is transmitted by the larval stage of the vector
rather than by the nymphal and adult stages, B. bovis prepatency (measured from the
time of tick infestation) is only slightly longer than that of B. bigemina. With
blood inoculation, the incubation time is usually 10-14 days; however, this can be
shortened by large inoculums.
Clinical Signs
Infections of B. bovis resemble, in many respects, those
seen with B. bigemina, but there are some characteristic differences.
Hemoglobinuria and hemoglobinemia are not as consistently seen in infections with B.
bovis, although they may occur (5,6). The level of anemia is frequently less severe,
but central nervous system involvement is more common. It is generally conceded that B.
bovis is the more virulent of the two organisms. This is particularly so in Australia
and to a lesser extent in Africa and the Western Hemisphere (6).
Animals commonly develop incoordination and depression and go down
with the head extended but later thrown back and have involuntary movement of the legs.
These signs are followed by death. Whereas the packed cell volume (PCV) in most fatal
infections with B. bigemina will be well below 10 percent, death commonly occurs
with B. bovis when the PCV is 12 percent or higher. When hemoglobinuria is seen,
the color is not nearly so dark, nor is the plasma following PCV determination so red. The
observed parasitemias in peripheral blood are usually much lower with B. bovis than
with B. bigemina.
Gross Lesions
Changes similar to those described for B. bigemina are
apparent.
Diagnosis
Field Diagnosis
Fever, anemia, jaundice, and hemoglobinuria are suggestive
clinical signs of babesiosis in cattle located in enzootic areas where Boophilus ticks occur. If these signs are also associated with erythrocytic destruction, the
diagnosis of babesiosis is strengthened. A positive diagnosis requires the identification
of the babesia on blood smears or either positive serologic tests, or transmission
experiments, or both. In addition, a technique of brain biopsies has been described that
has proven very useful in detecting and diagnosing B. bovis infections (9,22). The
characteristic low parasitemias in the circulating blood make this technique very useful
in improving the chances of seeing the organism. There is a marked concentration of
infected erythrocytes in the capillaries of the brain.
Specimens for the Laboratory
From each animal six blood smears should be made, air-dried and
fixed in methanol and/or a sample of whole blood in an anticoagulant and serum should be
collected. Serologic diagnostic techniques are similar to those described for B.
bigemina. Presently, immunofluorescence assay is the test of choice in the serologic
diagnosis of B. bovis (9).
Differential Diagnosis
In addition to those conditions mentioned for B. bigemina,
a differential diagnosis of B. bovis infection must include diseases producing
central nervous system (CNS) involvement such as rabies, other encephalitides, or toxic
effects that would produce similar CNS changes.
Prognosis
Once CNS signs become pronounced, the prognosis is poor.
Generally, B. bovis produces a somewhat more severe clinical response than does B.
bigemina.
Treatment
Chemotherapy is generally effective, with essentially the same
drugs as used for B. bigemina. B. bovis is usually somewhat more difficult
to treat, and a second treatment, or slightly increased dose rates, may be desirable.
Trypan blue is not effective against B. bovis (14). Imidocarb has been reported to
induce radical cures in vertebrate hosts. Babesia bovis-infected B. annulatus ticks, when placed on animals recently treated with imidocarb, apparently lost their
infectivity, for their progeny failed to transmit infection (15). Tick infection remained
following imidocarb treatment in a similar experiment with B. bigemina in B.
decoloratus (25).
Vaccination
Vaccines are used in a number of places where babesiosis is
endemic. Repeated passage of B. bovis in splenectomized calves results in the
attenuation of the organism (9,26). For many years, this attenuated vaccine has been
produced and successfully used in Australia for the prevention of B. bovis (6). In
some cattle (older, and producing dairy cows), chemotherapy may be indicated, but usually
the vaccine may be used without treatment.
The development of in vitro techniques for the cultivation of B.
bovis on bovine erythrocytes has led to the isolation of soluble antigens, which, when
combined with adjuvants, have proven immunogenic (27,28). These noninfectious vaccines,
although they do not prevent infection, appear to be responsible for moderating the
effects of infection. They do not produce as high a level of protection as is seen with
premunizing vaccines but are safe and do not yield carriers. In some instances, these
vaccines, although protective against homologous challenge, may not protect against
immunologic variants.
The continuous in vitro passage of B. bovis has been shown
to induce a level of attenuation similar to that seen with the passage of the organism in
splenectomized calves. Infection with this attenuated organism has been reported to
prevent clinical infection following a challenge with virulent B. bovis (29,30).
Control and Eradication
Eradication of the Boophilus vectors would eliminate
transmission of B. bovis which, over a period of time, would lead to its
eradication.
Sanitation and Disinfection
Aside from the efforts involved in the control and elimination of
the tick vector, sanitation and disinfection do not contribute to an abatement of the
disease incidence in enzootic areas. As with most blood diseases, however, care is
recommended in routine surgery (dehorning, castration, etc.) and needle vaccination
procedures to prevent the accidental transfer of blood from one animal to another, thereby
transmitting infection.
Other Bovine Babesias
Babesia divergens appears to be a serious pathogen for
cattle in the United Kingdom and northern Europe (11). It is a small species that
morphologically resembles B. bovis but is slightly smaller and tends to be located
at the periphery or margins of the infected erythrocyte. It is transmitted by Ixodes
ricinus, which becomes infected when the adult feeds on either a carrier or an acutely
infected host. All stages of the F1 and sometime F2 generation are infective and capable
of transmission (11).
Babesia divergens produces a disease syndrome similar to B.
bigemina and B. bovis; however, the cerebral form is rarely seen. Treatment
with those babesiacides previously discussed is effective.
The presence of Ixodes ticks (I. scapularis, I.
pacificus, and I. dammini) in the United States suggests the potential for this
babesia to become established here. Consequently, B. divergens is a pathogen that
should not be ignored.
Babesia jakimovi (a large species) is the causal agent of
Siberian piroplasmosis in cattle. It can also infect the Tartarean roe deer, Asian elk,
and reindeer. It appears to be transmitted transovarially by I. ricinus, but
mechanical transmission by gadflies is also suggested. Signs of infection and response to
treatment closely resemble B. bigemina (11).
Babesia major is a large species only slightly smaller than B. bigemina. This babesia is transmitted by Haemaphysalis punctata and
occurs in the United Kingdom, and northern Europe (11). It is essentially nonpathogenic
but can be induced to produce clinical effects and even death by serial passage in
splenectomized calves.
Babesia ovate, a large species, has been described in
Japan. It is apparently serologically distinct from B. bigemina. It is only mildly
pathogenic and responds to the same therapy used against B. bigemina (31).
Transmission in Japan is by the larvae of Haemaphysalis longicornis. No immunity or
cross-protection occurs with B. bigemina, B. bovis, or B. major.
Serologically it appears to be a distinct species.
Equine Babesiosis
(Equine Piroplasmosis)
Definition
Equine babesiosis is a febrile tick-borne disease of horses caused
by either Babesia caballi (Fig. 31 ), B. equi (Fig. 32) or both and
is generally characterized by erythrocytolysis leading to anemia, icterus, hemoglobinuria,
and death.
Geographic Distribution
Equine babesiosis is widely distributed throughout the tropics and
subtropics and to a lesser extent is known to occur in temperate regions.
Transmission
Babesia caballi is transmitted by ticks of the genera Dermacentor, Hyalomma, and Rhipicephalus and is passed transovarially from one tick
generation to the next. Experimental transmission of B. caballi under laboratory
conditions has been reported using Dermacentor nitens, D. albipictus, and D.
variabilis (9). The widespread prevalence of these ticks (D. albipictus and D.
variabilis), plus the presence or past presence of B. caballi in the United
States (32), creates an unanswered question of why B. caballi has not become more
widespread in the United States. Transmission of B. equi appears only to occur
transstadially (33). The vector or vectors of B. equi have not been identified in
the Western Hemisphere. Elsewhere, ticks of the genera Dermacentor, Hyalomma,
and Rhipicephalus appear to be involved.
Clinical Signs
The severity of clinical response is variable, and in many cases
spontaneous recovery may occur following a febrile response with no marked hemoglobinuria
or anemia (11). Other reports describe the response as more like that seen in cattle
babesiosis.
Diagnosis
A positive diagnosis requires the identification of the babesia on
blood smears, or positive serologic tests.
Specimens for the Laboratory
From each animal six blood smears should be made, air-dried and
fixed in methanol and/or a sample of whole blood in an anticoagulant and serum should be
collected.
Treatment
Both B. caballi and B. equi respond to the
babesiacidal drugs (Table 2), but B. equi is more refractory to
treatment than B. caballi (14). Imidocarb appears to be the drug of choice for
eliminating carrier status of infected horses. In the case of B. caballi, .2 mg/kg
given two times at a 24-hour interval appears effective. For the same effect in B. equi-infected
horses, 4 mg/kg is given four times at 72-hour intervals (14). This amount of drug
approaches the lethal dose for 50 percent of the inoculated group (LD50) of 32
mg/kg when given in two 16 mg/kg doses at 24-hour intervals (36). Side effects
characterized by restlessness, abdominal pain, sweating, rolling, heavy breathing, etc.,
are not uncommon following imidocarb treatment at these higher levels.
Vaccination
No efficacious vaccine for equine babesiosis is available.
Control and Eradication
Preventive Measures
Once a horse is infected, the carrier status may persist for an
extended period during which the carrier horse may act as reservoirs of infection. To
prevent the introduction of equine babesiosis into areas free of infection, restrictive
measures are sometimes imposed on imported horses.
Sanitation and Disinfection
Aside from measures involved in the control and elimination of the
tick vector, sanitation and disinfection do not contribute to an abatement of the disease
incidence in enzootic areas. As with most blood diseases, however, care is recommended in
routine surgery (castration, etc.) and needle vaccination procedures to prevent the
accidental transfer of blood from one animal to another, thereby transmitting infection.
Babesiosis of Other Domestic Animals
Sheep and Goats
Babesia motasi, a large species resembling B. bigemina morphologically, is infective for sheep and is transmitted by ticks of the genera Haemaphysalis and Rhipicephalus. This organism is widespread in the Old World, having been
identified in Europe, the Middle East, the former Soviet Union, Southeast Asia, and Africa
(11). B. motasi produces a mild clinical response characterized by fever and anemia
but alone is rarely responsible for significant death losses. Some strains are
transmissible to goats, but this is not a consistent observation.
Babesia ovis is a small species observed in sheep and goats
and occurs as a pathogenic entity in southern Europe and the Middle East (11). Rhipicephalus bursa has been shown to be a vector for this parasite, and I. ricinus and D.
reticulatus are suspected vectors. The signs of infection may resemble those described
for cattle with a febrile response, anemia, icterus, edema, and hemoglobinuria. Infections
are usually mild and often are inapparent.
Both B. motasi and B. ovis respond to one or more
those babesiacidal drugs referred to in Table 2 (14). Information on
these babesias is limited, and few serological and cross-immunological studies have been
made to clarify the identity of these intraerythrocytic parasites of sheep and goats.
Swine
Both Babesia trautmanni (large) and B. perroncitol (small)
occur in swine and, on occasion, are responsible for serious losses following infections,
producing signs not unlike those described for cattle (11). Swine babesiosis has been
described in the former Soviet Union, southern Europe, and Africa. In Africa, the wild
pigs (warthogs and bush pigs) are thought to be reservoirs. Several ticks (species of the
genera, Boophilus, Hyalomma, and Rhipicephalus) are suspected as
possible vectors. These infections generally respond to chemotherapy with those drugs
referred to in Table 2 (14).
Other Species
An array of other babesia species exist, and a great number of
vertebrate species are infected by one or more of these intraerythrocytic parasites.
Wildlife are also involved, but because these babesias are often relatively nonpathogenic,
they frequently go unnoticed.
Public Health
Of recent interest has been the occurrence of babesiosis in man.
At one time these human infections were thought to occur only in splenectomized
individuals, or those who were otherwise immunosuppressed. This is not, however, the case
where B. microti., transmitted by I. dammini (24), is involved.
GUIDE TO THE LITERATURE
1. GONZALES, E.F., TODOROVIC, R.A, and ADAMS, L.G. 1971.
Ultrastructural de Babesia bigemina. Rev. Inst. Col. Agropecuario, 6: 87-112.
2. DOLMAN, C.E. 1969. Texas cattle fever: A commemorative tribute
to Theobald Smith, Clio Medica ,4:131.
3. SMITH, T., and KILBORNE, F. L. 1893. Investigations into the
nature, causation, and prevention of Southern cattle fever. USDABAT, Bu1. 11:30.
4. GRAHAM, O.H., and HOURRIGAN, J.L. 1977. Eradication programs
for the arthropod parasites of livestock. J. Med. Ent., 13: 629-658.
5. RIEK, R. F. 1968. Babesiosis. In II. Infectious Blood
Diseases of Man and Animals, Weinman D, Ristic M (eds.), New York: Academic Press, pp.
219-268.
6. MAHONEY, D.F. 1977. Babesia of domestic animals. In Parasitic
Protozoa, Kreier JP (ed), New York: Academic Press, p. 152.
7. SMITH, H.A., and JONES T.C. 1957. Veterinary Pathology.
Philadelphia:Lea and Febiger.
8. MAHONEY, D.F., and SAAL, J.R. 1961. Bovine babesiosis: Thick
blood films for the detection of parasitemia. Austr. Vet. J., 37: 44-47.
9. KUTTLER, K.L. 1984. Babesiosis. Foreign Animal Diseases, USAHA,
Richmond, VA. pp.76-96.
10. McCOSKER, P.J. 1981. The Global Importance of Babesiosis. In Babesiosis,
Ristic M, Kreier JP (eds), New York:Academic Press. pp. 1-24.
11. PUMELL, R.E. 1981. Babesiosis in Various Hosts. In Babesiosis,
Ristic M, Kreier JP (eds), New York:Academic Press. pp. 25-63.
12. MAHONEY, D.F., and ROSS, D.R. 1972. Epizootiological factors
in the control of bovine babesiosis. Austr. Vet. J., 48: 292-298.
13. DEVOS, A.J., and POTGIETER, F.T. 1983. The effect of tick
control of the epidemiology of bovine babesiosis. Onderstepoort J. Vet. Res., 50: 3-5.
14. KUTTLER, K.L. 1981. Chemotherapy of Babesiosis: A review, In Babesiosis,
Ristic M, Kreier JP (eds), New York:Academic Press. pp. 65-85.
15. KUTTLER, K.L., GRAHAM, O.H., and TREVINO, J.L. 1975. The
effect of imidocarb treatment of babesia in the bovine and the tick (Boophilus
microplus). Res. Vet. Sci., 18: 198-200.
16. TODOROVIC, R.A., VIZCAINO, O.G., GONZALEZ, E.F., and ADAMS,
L.G. 1973. Chemoprophylaxis (Imidocarb) against Babesia bigemina and Babesia
argentina infections, Am. J. Vet. Res., 39:1153-1161.
17. TODOROVIC, R.A. 1974. Bovine babesiasis: Its diagnosis and
control. Am. J. Vet. Res., 35:1045-1052.
18. TODOROVIC, R.A., GONZALES, E.F., and ADAMS, L.G. 1975. Babesia
bigmina, Babesia argentina, and Anaplasma marginale: Coinfectious
immunity in bovines. Exp. Parasit., 37: 179-192.
19. DALGLIESH, R.J., CALLOW, L.L., MELLORS, LT., and McGREGOR, W.
1981. Development of a highly infective Babesia bigemina vaccine of reduced
virulence. Austr. Vet. J., 57: 8-11.
20. CALLOW, L.L., McGREGOR, W., PARKER, R.J., and DALGLIESH, R.J.
1974. Immunity of cattle to Babesia bigemina following its elimination from the
host, with observations on antibody levels detected by indirect fluorescent antibody test.
Austr. Vet. J., 50: 12-15.
21. REES, C.W. 1934. Characteristics of the piroplasms Babesia
argentina and B. bigemina in the United States. U. of Agri. Res., 45: 427-438.
22. LEEFLANG, P. 1972. Diagnosis of Babesia argentina infection in cattle. Austr. Vet. J., 48:72.
23. MORISOD, A., BROSSARD, M., LAMBERT, C., SUTER, H., and
AESCHLIMANN, A. 1972. Babesia bovis: Transmission par Ixodes ricinus (Ixodoidea) dans la plaine du Rhone. Schwiezer Arch. f. Tierheil., 114:387-394.
24. BROCKLESBY D. 1979. Human babesiosis. J. So. Afr. Vet. Assoc.,
50:302-307.
25. GRAY, J.S., and POTGIETER, F.T. 1981. The retention of Babesia
bigemina infection by Boophilus decoloratus exposed to imidocarb diproprionate
during engorgement. Onderest. J. Vet. Res., 48: 225-227.
26. CALLOW, L L., MELLORS, L.T., and McGREGOR, W. 1979. Reduction
in virulence of Babesia bovis due to rapid passage in splenectomized cattle. Int.
J. Parasit., 9: 333-338.
27. LEVY, M.G., and RISTIC, M. 1980. Babesia bovis:
Continuous cultivation in a microaeophilous stationary phase culture. Science, 107:
1218-1220.
28. KUTTLER, K.L., LEVY, M.G., and RISTIC, M. 1983. Cell culture
derived Babesia bovis vaccine: Sequential challenge exposure of protective immunity
during a 6-month postvaccination period. Am. J. Vet. Res., 44: 1456-1459.
29. YUNKER, C. E., KUTTLER, K.L., and JOHNSON, L.W. 1987.
Attenuation of Babesia bovis by in-vitro cultivation. Vet. Parast., 24: 713.
30. KUTTLER, K.L., ZAUGG, J. L. and YUNKER, C.E. 1988. The
pathogenicity and immunogic relationship of virulent and tissue culture adapted Babesis
bovis. Vet. Parasit., 27: 239-244.
31. MINAMI T., and ISHIHARA, T. 1980. Babesia ovate sp.n.
isolated from cattle in Japan. Nat. Inst. of Anim. Hlth. Quarterly, 20: 101-113.
32. SIPPLEL, W. L., COOPERRIDER, D. E., GAINER, J.H., ALLEN R.W.,
MOUW, J.E.B., and TAGLAND, M.B. 1962. Equine piroplasmosis in the United States.
J.A.V.M.A., 141: 694-698.
33. FRIEDHOFF, K.T. 1982. The piroplasms of Equidae, significance
for international commerce. Berl. Munch. Tierarztl. Wschr., 95: 368-374.
34. SCHEIN, F., REHBEIN, G., VOIGHT, W.P., and ZWEYGARTH, E. 1981. Babesia equi (Laveran 1901): 1) Development in horses and in lymphocyte culture.
Tropenmed Parasit., 32: 227-233.
35. ZWEYGARTH, E., AHMED, J.S., REHBEIN, G., and VOIGHT, W.P.
1983. Cell mediated immune response to Babesia equi transformed lymphoblastoid
cells in vitro. Zbl. Bakt. Hyg., 8: 281-289.
36. ADAMS, L.G. 1981. Clinicopathological aspects of imidocarb
dipropionate toxicity in horses. Res. Vet. Sci., 31: 54-61.
K. L Kuttler, D.V.M., M.S., Ph.D., Rt. 5, Box 1259, College
Station, TX
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