Home » other animals » Babesiosis in dogs: symptoms and treatment [wet medicine Krystyna Skiersinis

Babesiosis in dogs: symptoms and treatment [wet medicine Krystyna Skiersinis

Babesiosis is one of the most dangerous tick-borne diseases in dogs, which often ends in death.

Babesiosis in a dog from a tick

Babesiosis it occurs all over the world, but in some regions it is a serious epidemiological problem.

It is transmitted by ticks and is caused by protozoa of the genus Babesia, which penetrate red blood cells and break them down.

The most characteristic manifestation of babesiosis is therefore anemia, but - due to the fact that this condition is extremely dangerous in itself and entails a number of negative consequences - the overall picture of the disease consists of disruption of the functions of many internal organs, and thus a wide variety of clinical symptoms.

The older name of this disease - pyroplasmosis - is related to the morphology of protozoa, which in erythrocytes take a pear shaped shape ( "pear shaped ").

  • Causing factor
  • The occurrence of babesia protozoa
  • How is it infected??
  • And all because of the ticks

  • The pathogenesis of babesiosis
  • Babesiosis as protozoal sepsis
  • Symptoms of Babesiosis in Dogs
    • Babesia canis canis
    • Babesia vogeli
    • Babesia rossi
    • Babesia gibsoni
    • Babesia conradae
    • Babesia microti-like (Theileria Annae)
  • Complications related to babesiosis
    • Acute kidney failure
    • Cerebral Babesiosis
    • Blood coagulation disorders
    • Jaundice and liver changes
    • Immune-related haemolytic anemia (IMHA)
    • Blood thickening
    • Arterial hypotension
    • Cardiac disorders
    • Acute pancreatitis
    • Acid-base imbalance
  • Diagnosis of babesiosis in a dog
    • Differential diagnosis
  • Treatment of Babesiosis in Dogs
    • Causal treatment
    • Supportive treatment
  • Prognosis
  • Prevention of babesiosis
  • Immunoprophylaxis
  • Public health threat
  • Possible reasons for the more frequent diagnosis of babesiosis in dogs

Causing factor

In 1888, Romanian pathologist Victor Babes was the first to describe pear-shaped microbes he observed in cows' red blood cells showing symptoms of hemoglobinuria.

Then, the researcher found similar parasites in sheep erythrocytes.

Five years later, Americans Smith and Killborn conducting research on the so-called. cattle fever announced the discovery of the microbe Babesia bigemina.

In 1895 in Italy, Piana and Galli-Valero discovered in dogs erythrocytes protozoa very similar to those found in the course of Texas fever in cattle and named them Babesia canis (in honor of the first discoverer Victor Babes).

In Germany, the first description of these protozoa dates back to 1910.

Babesia found in military dog's red blood cells and described as "round lumps" that accumulated two or four in a single erythrocyte.

Babesiosis as a disease in dogs, it was first described in the United States in 1934 by Eaton, and in Poland in the Lublin region in 1966.

It is considered to be the oldest animal transmission disease described in Europe.

Today we know that the pathogens capable of inducing babesiosis in dogs are protozoa belonging to the genus Babesia, family Babesidae, order Piroplasmida, type Apicomplexa.

Babesia are protozoa that parasitize inside the red blood cells of vertebrates, and by developing and multiplying they destroy red blood cells.

Initially, the identification of these pathogens was based on the microscopic evaluation of blood smears collected from infected animals.

Considering the morphology of protozoa, these parasites in dogs have been divided into two main groups:

  1. Babesia canis - quite large, about 3-5 μm in size. These parasites in infected animals are usually found in erythrocytes, where they most often appear in pairs, are pear-shaped and usually joined by the narrow end. They can also take other forms, e.g. amoeboid or annular. Rarely found outside of blood cells (in blood plasma).
  2. Babesia gibsoni, which are slightly smaller than B. canis, about 1-3 μm in size. In erythrocytes, they appear in an oval or elongated form, in the amount of up to 5 parasites in the blood cell.

Thanks to the use of molecular biology methods, it has been clarified that within these two groups there are numerous Babesia species capable of causing disease in dogs:

  • Within the first group of protozoa, 3 subspecies of piroplasms were distinguished: Babesia canis rossi, Babesia canis canis and Babesia canis vogeli. In the United States, the so-called. large babesia that have not yet been named. All these protozoa have identical cell morphology, but differ in terms of geographic distribution, genetic structure, species of tick as a vector and virulence.
  • Within the second group, the smaller piroplasms are: Babesia conradae, Babesia microti-like (so named because of its similarity to Babesia microti, otherwise it is called Theileria annae. It was detected in the Pyrenees in Spain.) and other Theileria spp. However, even within a given species of babesia, there are strains that may differ from each other, e.g. virulence.

The occurrence of babesia protozoa

Protozoa Babesia spp | Source: Wikipedia

Both Babesia canis and Babesia gibsoni are found all over the world, but the geographic range and virulence of each species varies.

Parasites of the genus Babesia are mostly present:

  • southern Europe,
  • in Africa,
  • Asia,
  • North America,
  • Central and South America.

Babesia canis vogeli is found in tropical and subtropical regions and its geographic range includes:

  • Africa,
  • Asia,
  • Central, South and North America,
  • northern and central Europe,
  • Australia.

These protozoa are transmitted by the Rhipicephalus sanguineus tick.

They appear in the blood cells as large, single or paired pear-shaped trophozoites.

They are characterized by the lowest pathogenicity of all three subspecies of pyroplasma; the course of the disease is mild and the clinical symptoms are mild.

The course may be more severe in young animals.

Babesia canis canis

Within the Babesia canis canis strains there are pyroplasmas isolated in Europe and part of Asia.

They are medium-pathogenic protozoa, transmitted by ticks of the genus Dermacentor (in Poland Dermacentor reticulatus - meadow tick).

They have the typical morphological features characteristic of this group of protozoa: they are large, arranged in pairs or individually, pear-shaped.

In the dog's body, they cause temporary parasitemia and organ congestion.

Babesia canis rossi

Babesia canis rossi - are highly pathogenic strains that occur in South Africa.

They are transmitted by Haemaphysalis leachi ticks.

They cause highly advanced anemia or immune disease.

Babesia (large strain), identified in North Carolina (USA) causes hemolytic anemia, thrombocytopenia and leukopenia.

Babesia gibsoni

Babesia gibsoni pyroplasmas are found in northern and eastern Africa, southern Asia, Australia, southern Europe and the United States.

They are small ring-shaped protozoa (signet ring), usually found singly in red blood cells.

The relationship with the tick as a vector has not been confirmed, but is likely to be transmitted via:

  • Haemaphysalis bispinosa,
  • Rhipicephalus sanguineus.

They induce hemolytic anemia or chronic subclinical invasion with weight loss and weakness.

Small Babesia protozoa

Small Babesia protozoa discovered in California - are small in size, usually singly, sometimes in the shape of Maltese crosses.

The vector is unknown (most likely a wild reservoir host). They cause haemolytic anemia.

Babesia Annae

Babesia annae, discovered in northeastern Spain (the so-called. Spanish isolate) are small, usually singly.

The tick Ixodes haxagonus is likely to be involved in their transmission, but a wild-type reservoir host is also suspected.

They cause severe haemolytic anemia, eosinophilia, and sometimes renal failure.

Babesia equi

In Spain, the dog was also found to be infested by Babesia equi.

They are small, usually single protozoa causing haemolytic anemia. Unknown vector.

Babesia canis

In Poland, Babesia canis has been found so far, but due to frequent (also international or intercontinental) travels with a dog or cat, it is possible to invade new, "imported" species of piroplasmosis.

Babesiosis in Poland there is a focal point. This may be related to the uneven distribution of ticks in the environment, but also results from a greater or lesser presence in the area of ​​animals infected with Babesia spp.

The incidence of babesiosis to a large extent is related to the number of ticks in a given region.

In places where they appear particularly often, the incidence of this disease is much higher.

It should also be remembered that ticks can occur in small clusters of trees and shrubs - e.g.:

  • in parks,
  • in the meadows,
  • in the gardens,
  • in home and allotment gardens.

How is it infected??

Infection with protozoa occurs via ticks, which are the definitive hosts of Babesia pyroplasmas.

Protozoa need arachnids not only as a means of transport to be transferred to an intermediate host.

In ticks there is also a process called gamogony, as a result of which gametes are formed and the second, called sporogony, leading to the formation of sporozoites, i.e. forms of invasive protozoa capable of infecting vertebrates.

Due to the complex development cycle of protozoa, they need an intermediate host, which is dogs and other vertebrates, to close it.

The place where the asexual reproduction of parasites takes place is red blood cells.

As already mentioned, transmission of Babesia protozoa between hosts occurs through the injection of an infected tick.

The most important link in spreading an invasion is adult female (although Babesia canis occurs in all stages of development of ticks).

During arachnid blood sampling, protozoites penetrate the dog's blood and then adhere to the erythrocyte cell membrane.

In the process of endocytosis (local invagination of the cell membrane of blood cells), the red blood cells are absorbed into the interior.

Babesia canis multiplies inside erythrocytes by longitudinal division, resulting in the formation of merozoites and then polymorphic trophozoites.

As many as 16 merozoites can be formed in a single blood cell, but most often they occur singly or in pairs.

Trophozoites divide inside the red blood cell by longitudinal division, leading to the lysis of the red blood cell.

In the process of asexual reproduction (merogony), subsequent merozoites are formed, which leave the blood cells and after a short stay in the blood plasma, they penetrate the next erythrocytes.

Interestingly, merozoites can leave the blood cells without damaging them.

Babesia canis multiplication in the blood can take from several months to two years. After several generations, gamonts appear in erythrocytes - precursors of sex cells.

If such infected erythrocytes are collected by the tick during its feeding, pyroplasmas appear in the intestine about 10 hours after blood collection.

In the digestive tract of the parasite, blood cells are digested and all forms of Babesia, except gametes.

The gametes transform into gametes that penetrate the cells of the intestinal wall and combine to form a zygote, which then transforms into a moving ookinet.

Ookinets penetrate the intestine, crawl into various organs of the tick (hemolymph, muscles, glands, Malpigh's tubes, ovaries) where secondary ookinets are formed.

Then these forms penetrate the tissues of the salivary glands.

In the tick's salivary glands sporogony occurs and invasive forms for vertebrates - sporozoites, which are released into the tick's saliva.

During the next foraging, during food intake, sporozoites, along with the tick's saliva, are introduced into the bloodstream of the intermediate host (e.g. dog).

In order for Babesia canis to be transmitted, the arachnid must be foraging minimum 2-3 days.

But what happens with those ookinets that have penetrated into the ovaries of the tick??

They can remain dormant in the eggs as well as in the larvae developing from these eggs. This is called. transovarial transmission.

Further divisions of ookinets occur only in nymphs and imago of ticks. Therefore, once introduced into the environment, babesia can persist in the tick population for many years due to the transovarial and transstadial transmission of these parasites.

However, if the protozoa have not been transferred by a transovarial route, they are not in the larval stage.

Infection of puppies through the placenta is possible, but it is rare.

Since protozoa live in erythrocytes, it is possible that dogs can be infected by transfusion if the donor is the carrier of the disease.

Infection through direct contact between two dogs (e.g. while playing, licking each other) is not possible.

Interestingly, Babesia infection can also occur as a result of contact of wounds with infected blood.

Such situations often occur during dog fights, which is often found in the United States and Asia.

It should come as no surprise, then, that in the USA 93% of Babesia gibsoni and Babesia canis cases were American pit bull terriers.

And all because of the ticks

Tick

It is very loud about the deadly potential of ticks - they transmit diseases that are dangerous and often deadly not only for animals, but also for humans.

Few, however, know that ticks are

mites.

The largest, most organized and extremely adapted to the parasitic lifestyle of the mite.

They play a huge role in the spread of viral, bacterial and protozoal diseases. Their epidemiological importance as disease vectors is mainly due to:

  • long development cycle, which may span even several growing seasons;
  • transovarial and transstadial transport of microorganisms;
  • the viability of pathogens in adult ticks that remain in the diapause stage (winter period); This means that - in the case of transovarial transmission of germs - subsequent generations of ticks may be vectors of pathogens despite the lack of contact with the reservoir;
  • the presence of numerous reservoirs, which are individuals of many species of both wild and domestic animals, as well as birds.

Ticks transmit approximately:

  • 130 viruses,
  • 200 species of piroplasms and filaria,
  • 20 species of rickettsiae,
  • and many species of bacteria.

Tick ​​species differ in morphological features, living environment and types of hosts.

They undergo development with incomplete transformation, with the forms of larvae, nymphs and imago.

All these forms - apart from slight differences in the number of crotch legs and the degree of maturity of the reproductive organs - are similar to each other.

In temperate climates, they need three hosts during their life cycle, because they have to suck the blood of different hosts three times during their life cycle to reach the next developmental stages.

The feeding time varies, depending on the development stage of the tick - it can be 2-10 days.

It may take several hours from the moment you find yourself on the skin until the tick is injected. During this time, the parasite travels looking for a suitable place to collect blood.

The risk of transmission of pathogens increases with foraging and is highest after about 72 hours.

Immediately after puncture, they can be transferred:

  • tick-borne encephalitis virus,
  • Bartonella henselae bacteria,
  • Hepatozoon canis and Leishmania infantum.

After 3-4 hours of foraging, the risk of transmission of rickettsia increases:

  • Ehrlichia canis,
  • Anaplasma phagocytophilum,
  • Anaplasma platys.

After 16-18 hours, the likelihood of transmission increases:

  • Borrelia burgdorferi spirochetes,
  • Babesia canis protozoa.

The presented scenario concerns female ticks.

Males, eating much shorter but multiple diets, can transmit germs more quickly, especially as they switch hosts.

After collecting blood from the host, the female starts laying eggs. It usually does it on plants, from where the larvae that hatch attack the host (most often they are small mammals or reptiles).

The larvae feed on their prey for approx 206 days, then they fall off the host and transform into eight-legged nymphs.

The nymphs then attack the larger mammals, where they stay for approximately week, sucking blood all the time.

After this time, they leave their victim and remain dormant for some time, after which they transform into a mature form.

The latter is looking for another host on which it will be able to feed through 6-10 days.

The total length of the life cycle varies and depends largely on environmental conditions and host availability.

Development may even continue in temperate climates 4 years.

Ticks have adapted in a way to the lack of food - when the hosts are unavailable, individual development stages may be left without food from one year to even 4 years.

Ticks prefer environments with high humidity, low air circulation, slight temperature changes during the day and easy access to the host.

No wonder then that their distribution in different regions is not even.

The activity of ticks shows a certain seasonality.

They become active in March, April and forage to November.

During this period, two peaks in host attack intensity can be observed:

  • spring,
  • autumn.

However, it should be remembered that the risk of tick-borne diseases in temperate climates does not always occur in the spring months or in late autumn.

Unfortunately, the incidence of these diseases is also noted in other seasons of the year, although with a lower intensity.

It is also not uncommon that already in February the ambient temperature rises enough for these parasites to become active.

The hosts of Babesia canis in Poland can be:

  • Ixodes ricinus - common tick,
  • Ixodes hexagonus - hedgehog tick,
  • Dermacentor reticulatus - meadow tick,
  • Rhipicephalus sanguineus - canine tick,

Dragged from other countries:

  • Dermacentor marginatus - woodland tick,
  • Hyalomma marginatum - a wandering tick.

The primary hosts for Babesia canis in Europe (including Poland) are played by Dermacentor reticulatus and Rhipicephalus sanguineus.

The occurrence of babesiosis in the eastern and north-eastern part of the country is explained by the presence of the D tick in these regions. reticulatus. Babesia canis is considered to be transmitted to the dog by a meadow tick and Babesia vogeli by a canine tick.

Either B is the causative factor for babesiosis depending on the degree of spread of both arachnid species. canis, or B. vogeli.

Meadow tick Dermacentor reticulatus

It is the major vector of the Babesia canis protozoa in Europe.

Its range in Poland is discontinuous, and the parasite has been gradually spreading for 20 years.

It can be concluded that there are two populations of the meadow tick in Poland:

  1. The eastern population, which stretches from the eastern border of the country to central Poland and spreads further west,
  2. Western population, which progresses eastwards and covers the voivodships:
    • lubuskie,
    • Lower Silesia,
    • West Pomeranian,
    • Greater Poland.

Meadow tick is a species of the so-called. non-nesting.

This means that larvae and nymphs are associated with the burrows of their hosts, and domestic animals are preyed almost exclusively by adults.

The exception may be, for example,. burrow-exploring hunting dogs that may come into contact with juvenile species Dermacentor reticulatus.

Adult forms of ticks live in open areas, where, attached to the tops of tall grasses and perennials, they wait for their victims.

Meadow tick prefers moist areas covered with dense, tall vegetation.

It can be found in riverside areas, fallow lands near water reservoirs or on the edge of forests.

Unfortunately - now the area of ​​the meadow tick's occurrence has significantly widened.

It is most likely caused by the increase in the number and expansion of the elk, which is the main host for this arachnid. As the number of elk increased, the number of ticks feeding on them also increased, which resulted in the need to "search " for new hosts, which were deer, roe deer, lagomorphs (the parasite resides on them in the form of nymphs), and finally dogs and cats.

Thus, the meadow tick began to spread, moving from wetlands such as swamps, peat bogs and wet forests to less wet areas, even settling in cities.

The expansion of the meadow tick is also favored by global warming and changes in the way of maintaining the land, which lead to the creation of new habitats for adult forms of this parasite.

Currently, the meadow tick spreads fairly rapidly from east to west, which increases the number of Babesia canis infections in dogs.

Since this tick is characterized by two peaks of its activity: spring and summer, it is also in these periods that the incidence of canine babesiosis is more frequent.

However, its presence can often be observed also during light winters, when the air temperature does not drop below 0 ° C, and after thaws.

That is why anti-tick prophylaxis should be carried out all year round, and not only in the tick seasons.

Male meadow ticks repeatedly draw small amounts of blood to initiate spermatogenesis.

This means that both female and male can be involved in the transmission of pathogens to the host, but it is not fully known how long it takes for males to forage and what their contribution is to the transmission of Babesia canis.

Common tick Ixodes ricinus

It occurs throughout Poland.

It is a non-nesting species - this means that all developmental forms of ticks that are present in the environment can feed on domestic animals and humans.

These ticks can feed on about 300 species of mammals, birds and reptiles.

They are vectors of serious human and animal diseases, such as:

  • Lyme disease,
  • tick-borne encephalitis,
  • babesiosis,
  • anaplasmosis.

The habitat of the Ixodes ricinus tick is deciduous and mixed forests.The larvae remain in the litter and usually attack rodents and other small animals.

Nymphs and adult forms of ticks climb to a height of about 100-150 cm and, attached to the vegetation, wait for their hosts, thanks to which ticks can be transferred from forests to open areas and to city parks and other green areas.

However, Ixodes ricinus is sensitive to low levels of humidity and therefore cannot survive in open areas for long periods of time.

Tick ​​activity is observed in the environment from March to November, with activity peaks in late spring (late May to June) and the turn of summer and autumn.

Male Ixodes ricinus ticks do not draw blood. They are present on the host due to the fertilization of the female during her feeding.

The most important negative effects of these parasites on animals (and humans) are:

  • Mechanical action of the parasite, which is piercing into the skin. The morning dawn of tick feeding is the gateway to infection for pathogens, which can then lead to the development of skin inflammation.
  • Action that weakens the host's natural immune mechanisms. Ticks 'collaborate' surprisingly with the pathogens they transmit.
  • Serpins present in the saliva of ticks inhibit the differentiation and activity of helper lymphocytes with the CD4 (Th17) surface antigen, thus weakening the host's defense mechanisms. As a result, the antimicrobial defense is weaker, which may result in faster and easier development of the infection.
  • Eating - in the event of a large infestation of ticks, just feeding them can lead to anemia (especially if they feed on young, small hosts). However, infestations by ticks are generally of low intensity and clinical signs related to their direct action are rare.
  • Toxic effect, associated with the introduction together with tick saliva of various substances with analgesic, antipruritic, immunomodulating, anticoagulant and vasodilating effects. As a result, the host may experience various types of inflammatory and allergic reactions. The tick also introduces neurotoxins into the organism of its host, which inhibit the conduction of impulses through motor-sensory synapses.
    The invasion of these protozoa can lead to the so-called. tick paralysis, the symptoms of which are usually manifested several hours after contact with the tick. Symmetrical limb paresis, ascending muscle paralysis, and impaired motor coordination are then observed. As a rule, this condition disappears after several hours, but in some situations the respiratory muscles may be paralyzed, and the animal may even die. Tick ​​paralysis is caused in our climatic conditions by the taiga tick Ixodes persulcatus occurring in the north-eastern part of the country. In the Mediterranean, it is caused by ticks of the following genera:
    • Hyalomma,
    • Amblyomma,
    • Rhipicephalus,
    • in North America, Dermacentor andersoni.
  • Vector action. Infectious and invasive diseases transmitted by ticks are often the cause of serious diseases such as babesiosis, ehrlichiosis or Lyme disease. In many cases, these diseases lead to the death of the dog.

It should be remembered that ticks can be infected or infected with several pathogens at the same time.

These are so-called co-infections - the most commonly observed is the transmission of 2 different germs.

It also happens that one dog is fed by ticks of different species or those that carry different germs.

It is not uncommon for a dog to suffer from two tick-borne diseases, e.g. Lyme disease and anaplasmosis, and the clinical picture of these units overlaps, causing diagnostic and therapeutic difficulties.

The pathogenesis of babesiosis

Despite the decidedly negative impact of parasites on the animal, the direct action of Babesia protozoa plays a smaller role than the response induced by them in the form of a violent immune reaction and various biochemical processes.

Antibodies to Babesia antigens have already been found 5.-10. day after infection, with a maximum level of approx 3. week the duration of the invasion.

They can remain in the blood for many months, but after complete elimination of the protozoa they disappear relatively quickly.

Following infection, the host's immune system usually reacts significantly.

Babesia antigens - incorporated into the surface structure of erythrocytes - induce a humoral and cellular response, as a result of which the IgG1 antibodies coat red blood cells, and then intensified phagocytosis by activated erythrocyte macrophages - both those containing parasites and free.

Factors released by protozoa additionally destabilize erythrocyte cell membranes, but the effects of infection are not only disintegration of erythrocytes.

Parasites also increase the level of kinins, which leads to circulatory disorders and damages many organs, mainly the kidneys.

Hemoglobin is massively released from damaged erythrocytes - its metabolism is disturbed and metabolites are removed, which results in jaundice.

The main consequences of infection with the Babesia protozoa are therefore:

  • Hemolytic anemia. The presence of parasites in the blood and immunological processes cause the disintegration of the erythrocyte cell membrane, their breakdown (haemolysis) and - as a consequence, anemia. Breakdown of red blood cells can occur as a result of:
    • mechanical destruction of erythrocytes by protozoa escaping from the blood cells (some forms do not damage the erythrocyte membranes);
    • rupture of erythrocytes (due to the deposition of factors released by parasites on their surface, which destabilize the erythrocyte cell membrane);
    • erythrocyte disintegration by the formation of antigen-antibody immune complexes on the cell surface;
    • the action of the complement system and oxidizing factors (this may be a consequence of oxidative stress and increased peroxidation of cell membrane lipids). As a result, the structure of erythrocyte cell membranes is damaged, their continuity is lost and the ion permeability increases. As a result of increased peroxidation, oxidative ions accumulate in red blood cells. In the course of babesiosis, an increase in the concentration of malondialdehyde, which is a biomarker of lipid peroxidation, can be observed.
  • Fever - one of the first and constant symptoms of babesiosis.
    It is associated with the breakdown of a large number of red blood cells.
  • Hypoxia, i.e. tissue hypoxia that occurs during invasion, is a very important consequence of anemia. Hypoxia can lead to shock, vascular stasis, increased endogenous production of carbon monoxide, damage to hemoglobin and reduce the ability of hemoglobin to bind with oxygen. The organs that are most sensitive to oxygen deficiency are the brain, kidneys and muscles. Hypoxia may be an even more important factor in causing kidney damage than hemoglobinuria.
  • Metabolic acidosis - disturbance of the acid-base balance common in animals suffering from babesiosis; is caused by the production of lactic acid in hypoxic tissues.
  • Circulatory disorders caused by hypovolaemia and hypoxia in various organs (especially kidneys) lead to metabolic acidosis and cell death. These disorders are the result of an increase in kinin levels and the release of other substances that dilate the vessels and increase the permeability of the capillaries.
  • Hemoglobinuria results from the release of large amounts of hemoglobin from damaged red blood cells into the blood;
    after crossing the renal threshold, hemoglobin is excreted in the urine.
  • Bilirubinemia. Large amounts of released hemoglobin are converted into bilirubin in the cells of the reticuloendothelial system. Only part of it is then bound to blood proteins and excreted in the bile. The excess bilirubin remains in the blood vessels, causing jaundice.
  • Multiorgan dysfunction. In addition to the above-mentioned parasitic and immunological factors that affect the stability of the erythrocyte cell membrane, oxidative stress may also damage red blood cells and increase their susceptibility to phagocytosis. Oxidation processes stiffen the erythrocytes infected with protozoa, which slows down the movement of blood cells in the capillaries. The matter is further complicated by enzymes released by parasites that activate the formation of fibrinogen-like proteins (FLP). The arrangement of these proteins increases the viscosity of erythrocytes, which predisposes them to settling in the capillaries. This accumulation of erythrocytes in the capillaries contributes to acute anemia, but vascular stagnation also affects other organs and systems: the central nervous system, muscles and kidneys, leading to rhabdomyolysis and acute renal failure. Multiorgan lesions resulting from systemic inflammatory response syndrome (SIRS) include acute renal failure, liver damage, immune background haemolysis, pulmonary edema, rhabdomyolysis, and cerebral abnormalities. These conditions occur precisely as a result of a massive inflammatory reaction arising in the host organism infected with Babesia pyroplasmas, especially B. canis rossi.
  • Thrombocytopenia. It is a common condition accompanying babesiosis, and it occurs as a result of damage to platelets (due to immunological and hemolytic mechanisms). Often, dogs do not experience any visible effects of a bleeding disorder. Intravascular coagulation syndrome (DIC) is observed with severe infestation of Babesia canis rossi, which can lead to many dangerous complications. Thrombocytopenia is frequently seen in dogs infected with Babesia gibsoni.

Babesiosis as protozoal sepsis

Taking into account the disorders that occur in the course of babesiosis, it has been classified - like malaria in humans - as protozoan sepsis.

Sepsis is a syndrome of generalized inflammatory reaction as a result of an infection.

The diagnosis of the systemic inflammatory reaction syndrome is based on the following criteria (according to Okano et al.):

  • body temperature of 39.7 ° C or greater, or 37.8 ° C or less;
  • heart rate: 160 beats per minute or higher;
  • number of breaths: 40 breaths per minute or more;
  • leukocyte count: 4 G / L or less or also 12 G / L or more. Alternatively, the leukocyte count is normal, but the immature neutrophils account for a minimum of 10% of the total leukocyte count.

Severe sepsis is one accompanied by multiple organ failure syndrome. The criteria for this team are as follows:

  • renal dysfunction: creatinine concentration> 180 μmol / l (> 2 mg / dl);
  • liver dysfunction: ALT> 176 UI / l and ALP> 360 UI / l;
  • central nervous system disorders: < 9 punktów zmodyfikowanej skali śpiączki Glasgow. W tej skali dodaje się punkty uzyskane w ocenie aktywności motorycznej (1-6 punktów), odruchów z nerwów czaszkowych (1-6 punktów) oraz poziomu świadomości (1-6 punktów). Niewielka liczba punktów wskazuje na ciężkie uszkodzenie mózgu.
  • respiratory disorders: pulmonary edema or shortness of breath with discharge from the nose;
  • skeletal muscle damage: creatine kinase activity> 6000 UI / l.

Multiple organ failure syndrome can be diagnosed if the dog meets two or more criteria.

The most severe form of sepsis is septic shock.

It is otherwise known as "severe sepsis with refractory low blood pressure ".

This is a condition where systolic blood pressure remains below 90 mmHg despite adequate fluid therapy.

The prognosis for severe sepsis is cautious to evil, and with septic shock - bad.

The pathogenicity of pyroplasmas depends largely on the species and strain causing the invasion.

Other factors that influence the course of the disease are host dependent factors, e.g.:

  • age of the animal - in young puppies, under 8 months of age, the humoral response to infection is weak, therefore young animals are more susceptible to infection with piroplasms, and the disease progresses more rapidly;
  • the dog's immune status and the degree of reaction of the immune system to the infection;
  • breed and origin of the dog. Infections with Babesia canis are often observed in purebred dogs, less than 1 year of age, in individuals who have previously had babesiosis, and in those who have not received effective anti-tick prophylaxis;
  • co-infections caused by other microorganisms may obscure the clinical picture of the disease and cause diagnostic difficulties, as well as worsen the course of babesiosis;
  • splenectomy significantly aggravates anemia and parasitemia. The spleen plays a large role in disease control in dogs. After removal of the spleen, severe clinical symptoms develop quickly in canine babesiosis patients. Lack of spleen may be a significant factor that increases the risk of fatal babesiosis in both humans and animals.

As a rule, two types of disease are observed in animals suffering from babesiosis:

  • running with hemolytic anemia;
  • running with multi-organ dysfunction.

Symptoms of Babesiosis in Dogs

Symptoms of Babesiosis in Dogs

The incubation period of the disease varies from a few days to 2-3 weeks.

At this time, the symptoms of babesiosis are not yet revealed, but protozoa multiply intensively in the blood.

The severity of clinical symptoms can vary from moderate to very severe, often fatal.

Babesia canis canis

Babesia canis canis infestation is accompanied by a slight parasitemia, and the clinical symptoms of the disease are associated with hyperemia and macrophage infiltration in the organs.

The course of Babesia canis infestation is usually mild to severe.

Neither clinical symptoms accompanying the disease, nor haemolysis are proportional to the severity of parasitemia (low parasitemia does not guarantee that the course of the disease will be mild).

The disease usually takes place in the spring-autumn period, cases diagnosed in autumn are usually more severe than those diagnosed in spring.

Infection with Babesia canis in dogs is most often accompanied by the following clinical signs (in order of occurrence):

  • After a short time of incubation of the disease (on average 5-28 days after the tick bite), a high fever appears, reaching 40-42 ° C. This is one of the first symptoms that lasts about a week. In the later stage of the disease, internal body temperature returns to normal, and in some cases hypothermia is observed.
  • Apathy, weakness and accompanying lack of appetite, weight loss and dehydration are noticeable.
  • Soon signs of anemia appear as a result of the breakdown of red blood cells:
    • pallor of the mucous membranes,
    • decrease in red cell parameters (decrease in the number of erythrocytes, hematocrit value, hemoglobin content).
  • It is not uncommon to find circulatory and respiratory disorders, increased respiration and heart rate (as a visible effect of anemia).
  • As a result of intravascular haemolysis, hemoglobinuria sometimes occurs - although it is a pathognomonic symptom, it occurs relatively rarely (if the disease is diagnosed early, hemoglobinuria may not appear yet). Initially, the urine is pink, and as the disease develops, it becomes brown. Contains blood and bile pigments.
  • Urine tests reveal proteinuria.
  • You may notice yellowing of the skin and mucous membranes, which is a symptom of jaundice.
  • Haematological disorders are observed in the majority of dogs with babesiosis: severe thrombocytopenia (decrease in blood platelets), mild to moderate normocytic anemia, normocytic regenerative anemia, leukopenia (decrease in white blood cell count), neutropenia (decrease in neutrophil count), monocytosis. Increased liver enzymes, increases in urea and creatinine levels are frequently observed in serum chemistry. Possible electrolyte disturbances are: hypochloraemia, hypokalaemia and hyponatraemia.
  • Enlargement of the liver and spleen.
  • Sometimes the disease begins with diarrhea and vomiting.
  • It is also possible the occurrence of movement disorders, lameness, mobility problems, as well as muscle weakness (especially in the hind limbs).
    nervous disorders.
  • Sometimes the picture of the disease is accompanied by:
    • bronchopneumonia,
    • pulmonary oedema,
    • mouth infection,
    • gastroenteritis,
    • muscle and joint pain,
    • keratitis,
    • nerve palsy.

Among the symptoms listed, most are non-specific symptoms that may accompany other diseases.

Atypical symptoms may also be present, such as:

  • ascites,
  • swelling,
  • constipation,
  • diarrhea,
  • ulcerative gastritis,
  • hemorrhages,
  • hyperemia of the mucous membranes,
  • polycythemia (polycythemia),
  • runny nose and eyes,
  • breathing disorders,
  • inflammation of the masseter muscles,
  • pain in the temporomandibular joint,
  • pain in the sacral region,
  • central nervous system symptoms (attacks, seizures, ataxia, paresis).

Classification of clinical symptoms by duration:

Babesiosis can take the form of:

  • Hyperacute, rare.
    In this form, there is significant tissue damage, and the dominant symptoms are:
    • hypothermia (lowering body temperature),
    • shock,
    • coma,
    • disseminated intravascular coagulation,
    • metabolic acidosis,
    • death.
  • Acute, in the course of which, apart from non-specific symptoms such as fever and apathy, the following symptoms are observed:
    • hemolytic anemia,
    • jaundice,
    • enlargement of the spleen,
    • lymphadenopathy,
    • vomiting.
  • Chronic or subclinical. Chronic symptoms include:
    • intermittent fever,
    • partial anorexia,
    • lowering the overall condition of the body,
    • lymphadenopathy.

In most asymptomatic carriers, it is unlikely that clinical signs of babesiosis will be revealed.

In dogs that have survived the acute phase of infection without treatment, the chronic form may be completely asymptomatic. At this point, the morphology is back to normal.

This is a critical moment because it is a big diagnostic problem.

Dogs that are imported from southern countries are often in this phase of the disease, constituting a rich reservoir of protozoa for ticks, which, with subsequent bites, will transmit the disease to other animals.

Due to the course of the disease, we can distinguish uncomplicated and complicated babesiosis. This is the most general division of this pyrolasmosis:

  • Uncomplicated Babesiosis - as the name suggests, the disease affects animals that have not developed complications. Clinical symptoms are associated with acute anemia and, depending on its severity, may be weak, moderate or severe. However, it should be remembered that even uncomplicated babesiosis can develop into a more advanced disease. Thus, the most common observations are:
    • fever,
    • loss of appetite,
    • depression,
    • pallor of the mucous membranes,
    • enlargement of the spleen,
    • fast and high heart rate.
  • Complicated babesiosis characterized by impairment of the functions of many organs. Apart from the symptoms resulting from haemolytic anemia, the clinical picture of the disease may overlap with other clinical and laboratory changes complicating the course of the disease. Haemolytic anemia and the systemic inflammatory response syndrome (SIRS) accompanying complicated invasions lead to the multiple organ dysfunction syndrome (MODS). Quite rarely, there are gastrointestinal disorders, muscle pain, eye changes, upper respiratory symptoms, heart problems, limb necrosis, fluid retention, and chronic disease. These types of complications of babesiosis most often occur in dogs infected with Babesia canis rossi in South Africa.

Babesia vogeli

The course of Babesia vogeli disease is mild. Invasion is accompanied by moderate clinical signs.

In the United States, most dogs infected with B. vogeli are considered asymptomatic vectors.

The full development of clinical symptoms often occurs in dogs with a spleen removed, but also full-blown disease has been observed in very young animals and in elderly dogs with impaired immune function.

The spleen plays a very important role in controlling Babesia spp. Its lack causes the course of the disease to be much more severe, parasitemia greater, treatment more difficult, and the percentage of cases ending in death is much higher than in patients with a preserved organ.

In dogs with a properly functioning immune system in the course of Babesia vogeli disease, the following is observed:

  • regenerative hemolytic anemia,
  • fever,
  • lack of appetite,
  • apathy,
  • sometimes mild jaundice.

The results of laboratory tests (blood count and serum chemistry) in protozoan infected dogs are similar to those associated with Babesia canis infestation.

Babesia rossi

In turn, Babesia canis rossi, found in South Africa, is characterized by high pathogenicity.

It causes haemolytic anemia or a generalized inflammatory reaction.

Babesia rossi pyroplasmas are the most pathogenic of all Babesia protozoa species that are pathogenic to dogs.

Despite the fact that their place of occurrence is Africa, they are sometimes brought to Europe.

The activity of these pyroplasmas increases during the summer.

Piroplasmosis caused by Babesia rossi can take the form of:

  • Mild - with symptoms of anemia and good prognosis. With appropriate causal treatment, the response is rapid, but sometimes a blood transfusion may be necessary.
  • Complicated, with multiple organ failure and unfavorable prognosis. Animals require intensive care and the mortality rate is approximately 15%. Death is most often the result of brain damage, acute respiratory distress syndrome, or kidney failure. The main symptoms in dogs with complicated babesiosis include:
    • anemia,
    • jaundice,
    • low blood pressure,
    • dyspnoea,
    • vomiting,
    • diarrhea,
    • symptoms of pancreatitis,
    • muscle aches,
    • breakdown of striated muscle fibers,
    • ascites,
    • pulmonary oedema,
    • nervous symptoms.
  • Babesia canis rossi can cause acute or hyperacute disease. Invasion of this species of pyroplasma is accompanied by tissue hypoxia, shock, multi-organ failure and a relatively high mortality rate. In the course of the disease, the following are observed:
    • intense hemolysis,
    • renal failure and acid-base imbalance,
    • increased permeability of blood vessels due to the development of edema of non-cardiac origin.

Babesia gibsoni

Babesia gibsoni protozoa are often acute clinical symptoms.

Anorexia, haemolytic anemia, thrombocytopenia, enlargement of the lymph nodes and spleen are observed.

Anorexia, apathy, fever and vomiting are also common.

These symptoms can even lead to death (especially in puppies), but most treated animals with acute B disease. gibsoni is getting better. Hematuria is possible, as well as jaundice.

Babesia gibsoni infestation may be chronic or subclinical.

The symptoms are:

  • weight loss,
  • weakness,
  • anemia with (sometimes) jaundice and enlargement of the spleen.

In laboratory tests, the following is observed:

  • regenerative hemolytic anemia,
  • thrombocytopenia,
  • bilirubinemia.

Babesia conradae

Babesia conradae is found in the United States.

Invasion caused by these pyroplasmas is more severe than that caused by B. gibsoni and often results in the death of the animal.

Also, the clinical symptoms accompanying the disease are more intense, and the degree of anemia and parasitemia are more severe.

Babesia microti-like (Theileria Annae)

The first cases of dog diseases were detected in Spain.

The disease occurs mainly in the fall-winter season.

The main disorder is regenerative anemia with associated symptoms such as:

  • weakness,
  • fever,
  • acceleration of heart rate and breathing,
  • discoloration of the urine.

A common complication is the development of azotaemia.

Despite the similarity of clinical symptoms, it is extremely important to identify the causative agent of babesiosis not only from an epidemiological point of view, but also in order to be able to predict the disease as accurately as possible and implement appropriate therapy.

Complications related to babesiosis

Babesiosis does not always occur in its classic, uncomplicated form.

It is not uncommon for an animal to develop complicated babesiosis, and the patient and the doctor have to deal with not only protozoa as the cause, but also a whole range of adverse consequences resulting from the Babesia canis invasion.

Acute kidney failure

In animals suffering from babesiosis, urea levels may be abnormally high, but it is not conclusive evidence of renal failure.

It can occur in both complicated and uncomplicated cases of babesiosis, and its disproportionate increase in relation to creatinine is more indicative of lysis and degradation of erythrocytes as the cause of this state of affairs.

In renal failure, anuria or oliguria is a common symptom (despite proper hydration), and their damage is evidenced by proteinuria and the presence of renal rollers and tubular epithelial cells in the urine sediment test.

Therefore, in order to diagnose this (quite rare) complication of babesiosis, the measurement of urine volume, urinalysis and biochemical parameters of blood serum are taken into account.

Cerebral Babesiosis

We talk about it when a dog suffering from babesiosis is accompanied by neurological symptoms, e.g.:

  • incoordination with hind limb paralysis,
  • muscle tremors,
  • nystagmus,
  • pupil inequality,
  • loss of consciousness,
  • seizures,
  • stupor,
  • coma,
  • aggression,
  • rowing movements,
  • making various noises.

Blood coagulation disorders

They occur in both complicated and uncomplicated cases.

Advanced babesiosis-induced thrombocytopenia is one of the major changes, but it relatively rarely leads to clinically evident bleeding.

Intravascular coagulation syndrome (DIC) is possible, but its symptoms are difficult to recognize, given the nature of the ongoing disease process.

Jaundice and liver changes

Symptoms of liver damage include jaundice, elevated levels of liver enzymes, and an increase in bile acid levels.

Immune-related haemolytic anemia (IMHA)

It is the result of an increased breakdown of red blood cells as a result of the action of antibodies against the erythrocyte cell membranes, which are recognized as foreign and attacked by the body's defenses.

Unfortunately, even despite the use of antiprotozoal treatment, the destruction of red blood cells will continue.

The diagnosis of autoimmune haemolytic anemia is based on the agglutination test with a physiological solution.

In dogs with immune-related anemia, antibody-coated erythrocytes usually clump together (i.e. agglutinate), as can be seen from a simple office test.

A drop of EDTA blood is placed on the slide and one drop of physiological solution is added.

Rock the slide gently for 1-2 minutes and then check for agglutinates in the drop.

A positive result is the presence of autoagglutination in the blood.

Acute Respiratory Distress Syndrome (ARDS)

A fairly common complication of babesiosis, relatively severe in its course.

Revealed:

  • a sudden increase in the number of breaths (which may be caused by fever or acidosis),
  • breathlessness,
  • wet cough,
  • blood-stained, foamy discharge from the nose.

Blood thickening

In the course of babesiosis, blood thickens, which (most likely) results from the reduction of blood volume due to the displacement of fluids from the vascular bed into the extravascular space.

An important role in the pathogenesis of blood thickening may be played by the increase in capillary permeability, accompanying the systemic inflammatory response syndrome (SIRS).

Blood thickening can also occur as a result of other, coexisting complications, e.g.:

  • cerebral babesiosis,
  • DIC,
  • acute renal failure,
  • acute respiratory distress syndrome.

The processes accompanying severe intravascular haemolysis together with blood condensation lead to the condition known as "red jaundice ".

It is characterized by hyperemia of the mucous membranes and / or noticeable hemoglobinemia and hemoglobinuria, as well as high hematocrit values.

Arterial hypotension

Arterial hypotension quite often occurs in babesiosis, and the more advanced the disease, the greater the risk of hypotension.

Hypotension occurs as a result of vasodilation and reduction of their volume, which is the result of increased capillary permeability and / or dehydration, as well as heart failure.

Hypotension may play an important role in the pathophysiology of babesiosis as it promotes the deposition of pyroplasmas in capillaries.

With severe course of babesiosis, collapse and shock may even occur.

Cardiac disorders

Cardiac disorders are relatively frequently observed in babesiosis.

In the course of this disease (especially if complicated), there may be an increase in the level of troponin I (over 0.2 mg / dl) and the creatine kinase isoenzyme CK-MB (over 6.3 U / l).

The following changes are often found in ECG tests:

  • accelerated sinus rhythm (tachycardia),
  • deviation of the heart axis,
  • extended QRS complex,
  • change in T wave morphology,
  • I ° AV block,
  • ventricular agitation.

Echocardiography may show an increase in shortening fraction (FS%).

Acute pancreatitis

Acute pancreatitis often accompanies babesiosis - in retrospective studies, an increase in the level of lipase and / or amylase in the blood serum was found.

Pancreatitis is usually diagnosed approximately 2-3 days after starting treatment.

It is often accompanied by other complications, such as:

  • jaundice,
  • respiratory disorders,
  • hemolytic anemia of the immune background,
  • kidney failure,
  • blood thickening,
  • brain syndrome.

Pancreatitis may be a symptom of intestinal babesiosis.

Acid-base imbalance

Acid-base imbalance is often observed in canine babesiosis patients.

Usually, metabolic acidosis with a high anion gap is found, and some patients have simultaneous respiratory alkalosis.

Diagnosis of babesiosis in a dog

How to recognize the disease?

Diagnosing the disease can be difficult, especially given its varied course.

The diagnosis of babesiosis should include:

  • Focal occurrence of ticks in specific areas and their seasonality.
  • The presence of the dog in areas where ticks are located.
  • Earlier stay of the animal in a geographic area endemic to babesiosis.
  • Data from the interview, especially the previous finding of ticks on the dog. However, it should be remembered that a tick bite and its presence on the skin often go unnoticed.
  • Clinical symptoms noticed by the caregiver.
  • Demonstration of abnormalities during the clinical examination and such abnormalities in laboratory tests as:
    • in acute uncomplicated babesiosis:
      • haematological changes, e.g. damage to erythrocytes by parasites as a result of the immune system response, oxidative processes, gastrointestinal trauma and bleeding, masking haemolytic anemia;
      • pathological changes such as anemia and thrombocytopenia (thrombocytopenia is found more often than in ehrlichiosis). Initially, a slight degree of anemia (normocytic and normolourous) is diagnosed, and in the advanced stage of the disease, macrocytic, hypochromic and regenerative anemia is found. Reticulocytosis is also observed, the intensity of which is proportional to the severity of the anemia;
      • there is rarely hyperemia;
      • changes in the white blood cell picture seen in some dogs are: leukocytosis, neutrophilia, neutropenia, lymphocytosis and eosinophilia. A leukemia-like leukogram is very rare.
      • A positive result of the autoagglutination test in physiological solution is observed in some dogs suffering from babesiosis. 85% have a positive direct antiglobulin test (Coombs test).
      • Thrombocytopenia is a typical feature of babesiosis.
      • Serum biochemical parameters are usually normal. In the acute phase of the disease, elevated levels of bilirubin and LDH may be observed.
      • Hypokalaemia may occur in severely ill dogs, but it may be a consequence of a reduced potassium intake. With more severe course, hyperkalemia and hypoglycemia are possible.
    • Additionally, in dogs with moderate to severe babesiosis:
      • low levels of total protein and serum albumin,
      • decreased albumin to globulin ratio,
      • decreased levels of α-globulins,
      • increase in the level of α1-acid glycoproteins, which are the response of the acute phase of inflammation,
      • hyperglobulinemia occurs more often with the coexistence of Babesia canis and Ehrlichia canis infection,
      • In dogs with severe intravascular haemolysis, azotaemia and metabolic acidosis are found. It is associated with high mortality.
      • High levels of transaminase and alkaline phosphatase activity, and elevated bilirubin levels are seen in severely ill dogs. Hyperbilirubinemia is typical of the acute phase of Babesia canis infestation but not of Babesia gibsoni.
      • Urine tests show bilirubinuria, hemoglobinuria, proteinuria, and the presence of granular rollers.

The diagnosis is based on the identification of trophozoites inside Babesia spp. in the blood smear.

The presence of the parasite can be detected using the following methods:

  • microscopic examination of a smear of capillary or venous blood stained by the Giemsa method. The preparation should show trophozoites or merozoites inside the erythrocytes;
  • microscopic examination of a blood smear made using the linear compaction technique. This examination is more sensitive than the classic smear assessment;
  • microscopic examination of red blood cells located after centrifugation in a hematocrit capillary directly under the layer (the so-called. sheepskin coat) of leukocytes. This examination is also more sensitive than the classic smear;
  • microscopic examination of blood with the coarse drop method, however, the interpretation of the obtained image can be difficult.

Babesia canis are large protozoa, pear-shaped and usually found singly or in pairs.

Parasitemia is mildly severe during invasion, so searching for protozoa inside cells may be difficult.

It is necessary to make thin blood smears. To see more infected blood cells, blood for testing is taken from the capillaries of the ear or a claw.

If smaller forms are visible in the red blood cells, it can be assumed that we are dealing with Babesia gibsoni infestation.

Sometimes it is not possible to detect protozoa in smears despite visible disease symptoms.

This does not exclude the presence of an infestation, and often problems with finding pyroplasmas occur during the incubation of the disease.

Difficulties in finding piroplasms may result from the intensity of the invasion (with low, periodic parasitemia, it is difficult to demonstrate babesia), but also from the experience and accuracy of the person evaluating the preparation.

Pyroplasmas often do not have the typical pear-shaped shape, and erythrocytes often vacuolate, which makes it very difficult to assess the preparation.

It also happens that Babesia is found in blood cells "accidentally" in dogs that do not show clinical signs.

Inclusion bodies can sometimes be found in lymphocytes and neutrophils in blood from sick dogs. These are most likely phagocytosed fragments of red blood cells infected with parasites and the parasites themselves.

Since there are frequent difficulties in detecting the presence of Babesia protozoa, especially in chronically infected carriers, it is necessary to use serodiagnostic tests.

Serological methods such as indirect immunofluorescence (IFA), ELISA and OWD may be useful for detecting antibodies against Babesia canis antigens.

The enzyme immunoassay ELISA and dot-ELISA have been developed for the diagnosis of babesiosis.

The ELISA test is characterized by higher sensitivity and lower specificity than the indirect immunofluorescence test (IFA).

Serological tests are usually used to diagnose chronic disease. In acute babesiosis, they are unlikely to be used, because the detection of antibodies with these methods is possible only a few days after infection, when they appear at a detectable level.

In analytical laboratories to detect the presence of Babesia canis, the direct IFAT test method (. indirect fluorescent antibody test).

This method detects antibodies to Babesia canis and Babesia vogeli antigens in the dog's serum.

Nucleic acid detection - PCR method.

In the early stage of the invasion (in the acute phase), it may happen that the dog's body has not yet managed to produce detectable antibodies and the test result using the above methods is negative (apparently).

Therefore, if an acute infection is suspected, other, more detailed tests are necessary.

Genetic methods are considered to be the most sensitive and specific in diagnosing Babesia canis infestation.

The test is performed using the PCR method, examining DNA obtained from blood samples.

PCR not only allows for the final diagnosis, but also enables the identification of the protozoan species.

This method discovered a third species of Babesia protozoa found in the western regions of the United States, a new strain isolated from dogs in North Carolina, and strains isolated in Spain.

In Japan, thanks to PCR, protozoa similar to Babesia odocolei and Babesia divergens were detected in ticks obtained from dogs.

Differential diagnosis

The differential diagnosis should include, inter alia:

  • infection with rickettsiae, vectors of which are also ticks, e.g. Ehrlichia canis,
  • Haemobartonella canis infections,
  • leptospirosis,
  • warfarin poisoning,
  • invasion of gastrointestinal parasites.

In diagnostics, it may be important to identify the species of ticks feeding on the dog.

Treatment of Babesiosis in Dogs

Treatment of Babesiosis in Dogs

Babesiosis therapy should be two-fold:

  1. First of all, it is necessary to eliminate the disease-causing factor from the organism, namely Babesia spp.
  2. At the same time, proper function of internal organs should be ensured or restored, including combating anemia.

Before starting treatment, you should be sure that the cause of the disease is definitely Babesia spp.

The reason for this is the toxicity of anti-babesia drugs, which put a heavy strain on the internal organs, especially the liver.

Causal treatment

There are few drugs that are used to treat the causal babesiosis.

Highly toxic antiprotozoals with a low therapeutic index are used to combat this disease.

Clinical improvement is usually seen within 24 hours of starting treatment with antiprotozoal agents.

For the elimination of Babesia spp. apply:

Imidocarb dipropionate

It is a carbanilide derivative of the diminazene family.

It is effective against Babesia canis and to a lesser extent against Babesia gibsoni.

At recommended doses, it eliminates Babesia infestation and eliminates the invasiveness of parasitic ticks on treated dogs up to 4 weeks after administration.

In Poland, the only drug registered for the treatment of canine babesiosis is Imizol.

This medicine is a solution for injection that contains an active ingredient imidocarb.

Due to the long duration of action, it is recommended not only for the treatment but also for the prevention of babesiosis in various animal species, including dogs.

Effective at a dose of 3-6 mg / kg m.c (according to other data 5-6.6 mg / kg m.c.), which corresponds to 0.25 ml of the preparation / 10 kg m.c.

The dose may be repeated after 14 days.

The preparation is administered intramuscularly or subcutaneously, must not be administered intravenously.

The reaction to the applied treatment in the early phase of babesiosis is quick - new erythrocytes are formed as early as 12-24 hours after administration of the drug.

Side effects are rare, and if they do occur, the most common are:

  • transient salivation,
  • tearing,
  • vomiting,
  • diarrhea,
  • muscle tremors,
  • anxiety,
  • tachycardia,
  • dyspnoea.

The first adverse effects manifest themselves approximately 10 minutes after injection and include hypersalivation, injection site pain, vomiting, diarrhea and apathy.

They usually go away on their own.

In more severe cases, atropine sulfate is used as an antidote.

Sometimes delayed reactions develop around 10-12 hours after administration and usually include:

  • seizures,
  • strong apathy,
  • fever,
  • arrhythmia.

Dogs can become infected with Babesia species that are not specific to them, e.g. Theileria equi or Babesia caballi.

This may make it difficult to treat dogs suffering from babesiosis using standard doses of imidocarb.

Diminazene Aceturate

Diminazen is one of the most effective drugs for the treatment of Babesia canis, unfortunately not available in Poland.

It is an aromatic derivative of diamidine.

It affects the transformation of sugars and inhibits the aerobic processes in the organism of the parasite, inhibits the synthesis of gout, damages the membranes of cellular structures and causes the breakdown of the cytoplasm of protozoa.

Administration of the drug does not always lead to complete elimination of the infection (even in high doses).

Babesia canis pyroplasmas are more susceptible to diminazen than Babesia gibsoni.

Dogs are more sensitive to this drug than other animal species and the most common side effects caused by it are:

  • ache,
  • swelling at the injection site,
  • digestive system irritation,
  • neurological symptoms.

The preparation containing diminazene is Fatrybanil - it is administered at a dose of 1 ml of the drug per 15 kg m.c. deep intramuscularly.

The antipyrine contained in the preparation has antipyretic and analgesic properties.

Berenil is another preparation containing the active substance diminazene.

It is recommended mainly for cattle and dogs, but in Poland this preparation is not registered.

At a therapeutic dose, this formulation improves the clinical condition of dogs, but often does not completely eliminate protozoa.

In the event of an overdose, the following may occur:

  • nystagmus,
  • incoherence of movements,
  • even death.

The dose for a dog is 3.5 - 5 mg / kg m.c. diminazene aceturate, (1 ml / 10 kg m.c.) administered once, deep intramuscularly.

It is not recommended to administer it in severe forms of the disease, as it can lower blood pressure and has an anticholinergic effect.

Phenamidine isothioate

The commercial preparation - Oxopirvedine, intended for use only in dogs, contains in its composition fanamidine (showing antiprotozoal and antiseptic properties) and oxomemazine, which is a strong antihistaminic (it reduces the side effects caused by phenamidine, such as drooling, vomiting, swelling in injection site).

The preparation is administered subcutaneously at a dose of 15 mg / kg m.c., which corresponds to 1 ml of the drug / kg m.c.

As a rule, a single dose is sometimes sufficient, but sometimes it is recommended to repeat the injection after 24-48 hours.

Pentamidine isothioate

Pentamidine interferes with the synthesis of DNA, RNA and protozoa proteins.

Lomidine is a preparation containing pentamidine and can be used in animals as a medicine against various protozoal infections.

In the case of canine babesiosis, pentamidine isothionate is administered at a dose of 16.5 mg / kg m.c., which corresponds to 1 ml of the preparation per 10 kg m.c., deep intramuscularly.

The drug is highly effective, but many dogs experience side effects, sometimes severe.

Usually, a single administration of the preparation is sufficient, but sometimes it is necessary to repeat the dose after 24-48 hours.

The drug must not be administered subcutaneously or intravenously.

Lomidine can be administered intraperitoneally after 10-fold dilution with normal body fluid.

Chinuronium

Quinuronium sulfate (Acaprin) was administered subcutaneously at a dose of 0.025 ml per 5 kg m.c. after dilution with water 1:10.

It was withdrawn from production because after its use, side effects were often observed, such as:

  • motor disorders,
  • muscle tremors,
  • lying down,
  • shallow breathing,
  • drooling,
  • involuntary defecation.

Atovaquone

Mepron, containing atovaquone, is a medicine that is used to treat pneumonia in people with a compromised immune system (HIV-infected).

The effectiveness of this drug was tested in dogs against Babesia gibsoni infestation.

Atovaquone administered to dogs for 10 days orally every 8 hours at a dose of 13.3 mg / kg m.c. together with azithromycin (administered once daily at a dose of 10 mg / kg m.c.) eliminated Babesia gibsoni infection or lowered the level of parasitemia.

In many countries, this drug is difficult to obtain and treatment costs are high.

The drug should be used in conjunction with other drugs, because when used alone, it was insufficient to completely control the disease - often after 30 days from the start of treatment, Babesia gibsoni invasions returned.

1% trypan blue solution

It is effective in treating dogs with moderate symptoms of Babesia canis infestation.

It prevents the penetration of protozoa into red blood cells.

In dogs, it is administered intravenously at a dose of 10 mg / kg m.c. as a 1% solution.

As there are almost no side effects after its use, its use is recommended in the treatment of the early stage of severe babesiosis.

Unfortunately, it does not completely eliminate the infection, and its treatment results in a blue color of tissues and blood plasma.

In the absence of available anti-bacterial drugs, persistent supportive treatment combined with oral administration of clindamycin is recommended.

Clindamycin is a lincosamide antibiotic.

It is administered orally at a dose of 25 mg / kg m.c. every 12 hours for 7-21 days until healed.

It is now often recommended.

Clindamycin is the drug of choice for the treatment of human Babesia microti infection. When administered to dogs at the recommended dose, it resulted in relief of anemia and other clinical signs of babesiosis.

Unfortunately - in dogs treated with clindamycin there were no clinically significant differences in the severity of parasitemia, as well as in the level of IgG antibodies.

However, degenerative morphological changes have been observed in circulating pyroplasmas.

Doxycycline at a dose of 10 mg / kg m.c. administered every 12 hours for 7-10 days successfully counteracted or reduced parasitemia in dogs treated while they were infected.

Resistance to the most commonly used anti-babesiosis drug in Poland - imidocarb - occurs sporadically, but it is a serious problem, because when this drug does not work, our options in treating the disease are very limited.

What about this situation?

An alternative could be:

  • Administration of chloroquine, which inhibits protozoan DNA synthesis. It is an anti-malaria drug. It works by increasing the pH in protozoan cells. It also affects the destruction of hemoglobin in Babesia's food aquatic warblers, thereby releasing heme, which has a lytic effect on cell membranes. It is administered at a dose of 10 mg / kg orally (after 6 hours, 5 mg / kg m.c., then 5 mg / kg 4 times at 24 hour intervals).
  • Administration of diminazene, which disrupts the aerobic processes of pyroplasmas.
  • Administration of clindamycin pentamidine, amicarbalide, metronidazole or trypan blue.

All of them are, unfortunately, much less effective in fighting invasions compared to imidocarb. That is why it is sometimes combined with one of the above drugs in therapy.

In fact, Babesia resistance may develop to any of the therapeutic agents listed.

Supportive treatment

Supportive treatment is an extremely important element in the treatment of babesiosis.

The selection of supportive therapy should be based on appropriate assessment and continuous monitoring of the patient's condition.

Appropriate laboratory tests should be performed regularly during treatment, and if complications occur, they should be treated appropriately.

Supportive therapy includes:

  • Intravenous administration of multi-electrolyte fluids in the amount of 40-80 ml / kg m.c. It is justified as it removes the symptoms of hypovolemia and improves kidney function.
  • The administration of corticosteroid preparations is controversial because the desirability of steroid administration is often questioned. Although they eliminate the symptoms of shock and counteract some immune-related symptoms, long-term use of glucocorticosteroids may predispose the animal to other infections, and also contribute to the recurrence of babesiosis.
  • Blood transfusions. The indication for transfusion is severe disease when the accompanying anemia is life-threatening. The decision to transfuse should be based on clinical symptoms, medical history, and haematological findings. Symptoms that may require a blood transfusion include:
    • increased heart rate (tachycardia),
    • rapid breathing (tachypnoea),
    • fast and high heart rate,
    • weakness and collapse.
      You should also take into account how quickly symptoms worsen, as well as the degree of regeneration of red blood cells. The most frequently considered indicator of anemia is the hematocrit value. Usually, a transfusion should be considered when hematocrit is 15% or less, but should always be related to current clinical symptoms and medical history. In ambiguous situations, you can also rely on the number of red blood cells and hemoglobin content. When the hematocrit drops below 10%, transfusion becomes a necessity. In the treatment of dogs with babesiosis, administration of red blood cells alone is preferable (plasma administration is not necessary in most dogs). Giving fresh whole blood to sick dogs improves oxygenation, acid-base balance and supports the exchange of not fully functional hemoglobin for normal. Intravenous infusion of heparin is used to prevent the formation of intravascular embolism. Dopamine (10 μg / kg m.c.) by intravenous infusion. In the elimination of acidosis, it is helpful to use intravenous infusions (several times a day) of sodium bicarbonate in a 5% solution.
  • Drugs to support the liver, vitamins, adequate nutrition.
  • Treatment of complications after Babesia canis infestation such as:
    • acute kidney damage with consequent acute renal failure,
    • hyperhydration with unrecognized oliguria,
    • hyperkalemia,
    • severe metabolic acidosis,
    • acute hepatitis with jaundice,
    • sepsis,
    • nephrotic syndrome (very rare),

Renal replacement therapy is indicated when the daily increase in urea exceeds 40 mg despite diuretic therapy and fluid therapy, and additionally there is oliguria or anuria.

Hemodialysis is a method of purifying blood from undesirable substances, excess water and electrolytes based on the phenomena of diffusion, ultrafiltration and convection. Thanks to its use, the chance of restoring the body's normal homeostasis and restoring kidney function increases.

Apart from the key factor, which is an effective antiprotozoal drug, the therapeutic success is also extremely important to the supportive therapy and the speed of introducing the treatment.

Prognosis

The prognosis of babesiosis depends on many factors, including the severity of the disease, the severity of anemia, the degree of involvement of internal organs, and the response to treatment.

The best prognosis is when Babesia canis infestation is detected early before anemia has developed.

In severe or complicated babesiosis, treatment must be more intensive.

The following scenarios are possible:

Cure with complete elimination of protozoa.

Withdrawal of clinical symptoms, but pyroplasmas remain in the erythrocytes, capable of causing periodic relapses (often in winter).

Dogs that eliminate the initial infection but remain protozoan carriers may experience a relapse of babesiosis in stressful situations such as illness, pregnancy, or even surgery.

The disease becomes chronic, which results in damage to various organs, mainly the kidneys.

Often the disease leads to the death of the animal, usually due to hemolytic anemia (which results in shock) or due to intravascular coagulation syndrome.

Death may be the result of metabolic acidosis, which develops in the absence of sufficient oxygen.

It also happens that the patient dies as a result of azotaemia, leading to uremia and intoxication of the body.

It is caused by damage to the glomeruli by elements of damaged erythrocytes, antigen-antibody immune complexes, or both.

Prevention of babesiosis

The availability of specifically acting drugs against Babesia protozoa in Poland is very limited.

Veterinarians in most cases only have Imizol to which resistance is increasingly observed.

Therefore, disease prevention has become an overriding goal, although it is quite a difficult endeavor.

Treating tick infestations is the primary way to prevent outbreaks in dogs:

  • Limiting contact of dogs with ticks (final hosts of Babesia spp.) by avoiding potential tick habitats.
  • It is extremely important to check the skin and coat frequently. Ticks draw blood for a minimum of 2-3 days before parasite transmission occurs, so prompt removal of the parasite can be a key factor in preventing infection.
  • The use of anti-tick preparations in the form of collars, sprays, tablets, drops applied to the neck, etc., containing protozoal substances, e.g.:
    • fipronil 6.7-7.5 mg / kg m.c. in the form of a spot-on or spray;
    • fipronil 6.7 mg / kg m.c. + metoprene 6 mg / kg m.c. + amitraz 8 mg / kg m.c. spot-on;
    • permethrin 100 mg / kg m.c. + pyriproxyphene 0.75 mg / kg m.c. spot-on;
    • dinotefuran 6.4-8.5 mg / kg m.c. + pyriproxyphene 0.6-0.8 mg / kg m.c.+ permethrin 46.6 -62.2 mg / kg m.c. spot-on;
    • propoxur 125 mg / kg m.c. + flumethrin 28 mg / kg m.c. collar;
    • afoxolaner 2.5 mg / kg m.c. oral product;
    • fluralaner 25-56 mg / kg m.c. oral product;
    • soralaner 2-4 mg / kg m.c. oral product.

Examples of preparations used against ticks in dogs include:

  • Advantix (Bayer Animal Health), containing imidacloprid and permethrin.
  • Bravecto (Intervet International) - chewable tablets containing fluralaner.
  • Controline (Zoetis Polska) - a spot-on solution containing fipronil.
  • Duowin Contact (Virbac) - spot-on solution containing permethrin and pyriproxyfen.
  • Effipro (Virbac) - a spot-on or spray-on solution containing fipronil.
  • Ektopar (Vet-Agro) - a spot-on liquid containing permethrin.
  • Effitix (Virbac) - a spot-on solution containing fipronil and permethrin.
  • Fiprex (Vet-Agro) - Spot-on solution or spray solution containing fipronil.
  • Flevox (Vetoquinol Biowet) - spot-on solution containing fipronil.
  • Foresto (Bayer Animal Health) - collar containing imidacloprid and flumethrin.
  • Insectin (Biowet Puławy) - a powder to be applied to the skin, containing permethrin.
  • Kiltix (Bayer Animal Health) - collar containing propoxur and flumethrin.
  • Nexgard Spectra (Boehringer Ingelheim) - chewable tablets containing afoxolaner and milbemycin oxime.
  • Prac-tic (Elanco Europe Ltd.) - a spot-on solution containing pyriprole.
  • Simparica (Zoetis Belgium) - chewable tablets containing sarolaner.
  • Vectra 3D (Ceva Sante Animale) - spot-on solution containing dinotefuran, pyriproxyfen, permethrin.

Fighting ticks in the natural environment is not recommended, due to the fact that acaricides also act on other organisms.

Before introducing new dogs to breeding, they should be serologically tested, and if an infestation is detected, appropriate treatment and quarantine should be applied.

Immunoprophylaxis

Pirodog vaccine

Pirodog vaccine developed in France, used in Europe (not available in Poland).

It contains Babesia metabolic antigens, saponin as an adjuvant and is formalin preserved.

The vaccine is administered before the start of the tick season, twice a month, repeating vaccination annually.

The vaccine (according to reports) does not protect the entire population of dogs against infection and clinical signs. And indeed - attempts to introduce the Pirodog vaccine in Poland ended in failure due to its low effectiveness.

Interestingly, it showed a good protective effect in France and Switzerland.

Nobivac Piro vaccine

Nobivac Piro for the active immunization of dogs from 6 months of age.

It contains Babesia canis canis and Babesia canis rossi antigens.

It makes it possible to reduce the clinical symptoms of babesiosis.

Dogs gain immunity 3 weeks after vaccination, injection is repeated after 3-6 weeks.

Immunity lasts for about 6 months.

Although vaccination may not prevent an infestation of B. canis, however, it is often milder in vaccinated dogs.

Chemoprophylaxis

Chemoprophylaxis is the administration of drugs against Babesia canis when the risk of infection is high (e.g. in areas endemic to babesiosis in the tick season).

The drug of choice is Imizol (imidocarb), administered subcutaneously or intramuscularly at a dose of 0.5 ml of the drug per 10 kg m.c. (i.e. 6 mg of active substance per 1 kg of m.c.).

A single injection protects dogs for 4-6 weeks.

The drug may be repeated after this time if necessary, but the use of multiple doses is associated with a greater risk of intoxication.

The incidence of subclinical babesiosis may result in the persistence of active immunity for some time.

Antibody titres against Babesia canis gradually decline between 3 months of age. a 5. one month after infection.

Dogs are resistant to infection with the same strains for 5-8 months after infection.

There is no cross-resistance between babesia strains, and a positive antibody titer is not a guarantee in the event of infection with a different strain of Babesia canis.

Since Babesia pyroplasmas can be transmitted during blood transfusions, it is extremely important to check blood donors. All blood-sourced dogs should be tested for babesiosis.

The PCR method is very effective in detecting infected dogs.

Public health threat

Babesiosis is also dangerous to humans, although it is rarely diagnosed in Poland.

It is found all over Europe, in the northeastern and western states of the United States, and single cases have been reported in Africa and Mexico.

In most cases, invasions are asymptomatic or mildly severe.

However, there are also severe and even fatal cases of the disease.

People most at risk of developing babesiosis are people after splenectomy (removal of the spleen) and the elderly, over 55. age.

None of the Babesia species are considered specific to humans and, to date, no cases of human infection with protozoa of the genus Babesia occurring in dogs have been reported.

In humans, invasion is caused by species:

  • Babesia divergens,
  • Babesia microti,
  • Babesia venatorum,
  • Babesia duncani.

Humans are random hosts for different species of these protozoa if they are bitten by an infected tick.

In the United States, Babesia microti is the main species of pyroplasma attacking humans, and the invasion vector is the tick Ixodes scapularis (dammini), which is also a carrier of Lyme disease.

The disease, the main feature of which is anemia, is associated with flu-like symptoms.

The most severe human babesiosis are those caused by Babesia divergens in Europe and Babesia equi in the United States.

They most often affect people after splenectomy and are usually fatal.

Reports of babesiosis in humans caused by Babesia bovis or Babesia canis (i.e. species inhabiting domestic animals) have not been well documented.

Babesia species responsible for causing disease in dogs (B. canis and B. vogeli) do not pose a threat to humans.

In turn, the most common species in Poland are Babesia microti and Babesia divergens. They rapidly multiply in erythrocytes, leading to their breakdown.

As a result, the parenchyma of the kidneys and liver are destroyed, resulting in their failure.

Possible reasons for the more frequent diagnosis of babesiosis in dogs

Babesiosis in dogs is now diagnosed much more often than it was a few dozen years ago.

Why is this happening?

The reason for this state of affairs is several factors related to the etiological factor itself, its vectors, as well as intermediate hosts (dogs), as well as diagnostic possibilities:

  • Greater mobility of people and animals contributes to greater exposure of dogs to the threat posed by ticks. Frequent walks in the forest and trips to the areas where ticks live are factors that facilitate dog contact with the tick, and thus increase the risk of Babesia spp infestation.
  • More frequent trips of owners with dogs to exotic countries, where protozoa reside, which have not been recorded in Poland so far, and are capable of causing disease.
  • Rapid increase in the tick population due to climate change and greater host availability.
  • Resistance of ticks to commonly used acaricides.
  • Increasing number of doctors specializing in the treatment of dogs.
  • Greater awareness of animal keepers, universal access to information, easier exchange of experiences between dog keepers (e.g. via online forums).
  • Greater knowledge of doctors.
  • Greater opportunities in laboratory diagnostics, including the development of new molecular biology techniques. They allow not only to detect but also differentiate individual Babesia species that are pathogenic to dogs.

Despite the fact that babesiosis is a disease that is already quite well understood, it still provides doctors with many diagnostic and therapeutic problems.

The reason for this may be the high genetic variability of protozoa, which in turn results in a different course of the disease and an unpredictable reaction to drugs.

The procedure of key importance for the prevention of babesiosis is therefore the control of ticks, which are the most important link in the transmission of not only babesiosis, but also other, often equally dangerous diseases, such as Lyme disease or anaplasmosis.

Unfortunately, ticks also become resistant to many active substances present in acaricidal preparations and many of them - fantastically effective just a few years ago - nowadays more and more often fail the exam.

Therefore, when we notice that the collar or the skin solution that was used in our dog has ceased to protect, it is necessary to change the product to one that contains a different active substance.

In the season of ticks occurrence, it is recommended to conduct "double " prophylaxis, i.e. anti-tick collar with spot-on preparation.

When choosing such a preparation, it is worth consulting a veterinarian, because doctors know the current epizootiological situation, know which products are no longer effective in a given area and are able to skillfully select the appropriate preparation that will be most effective in a particular animal.

Remember - treated babesiosis almost always ends with a cure. Often untreated babesiosis ends in death.

Therefore, if you notice any symptoms that make you suspect this disease, take your dog to your vet immediately.

The time of starting the treatment is very important, because the early introduction of the therapy can protect our client from the negative consequences and complications of Babesia canis invasion.

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