Blood Smear Analysis: Babesiosis

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Blood Smear Analysis: Babesiosis



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Babesiosis

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All potentially relevant citations were subjected to a full-text review, using predefined inclusion and exclusion criteria that were tailored to meet the specific population, intervention, and comparator for each clinical question. Conference abstracts and proceedings, letters to the editor, editorials, review articles, and unpublished data were excluded from the evidence that served as a basis for graded recommendations.

The results of the literature search were thoroughly reviewed by the technical team for final selection of the relevant articles. Panel members reviewed the literature search for accuracy. Evidence summaries for each question were prepared by the technical team. The risk of bias was assessed by the technical team using the Cochrane risk of bias tool for randomized controlled trials [ 42 ], the Newcastle-Ottawa scale NOS for nonrandomized studies [ 43 ] and QUADAS-2 tool for diagnostic test accuracy studies [ 44 ].

The certainty in the evidence was initially determined for each critical and important outcome, and then for each recommendation using the GRADE approach for rating the confidence in the evidence [ 45 , 46 ] [ Figure 1 ]. Evidence profile tables and quality of evidence were reviewed by the guideline methodologists Y. The summaries of evidence were discussed and reviewed by all committee members and edited as appropriate.

The final evidence summaries were presented to the whole panel for deliberation and drafting of recommendations. Literature search strategies, the PRISMA flow diagram detailing the search results, data extraction and evidence profile tables, and additional data such as meta-analysis results when appropriate can be found in supplementary materials. Ranking of the outcomes by importance for decision-making was determined by consensus for each PICO question. In situations where a PICO question compared the use of an antimicrobial regimen to no antimicrobials, if the beneficial effects of the antimicrobial regimen were uncertain, undesirable outcomes would usually be ranked higher in importance than if benefits were certain ie, ranked as critical for decision-making rather than important.

Moreover, in situations where a PICO question compared the use of a specific antimicrobial regimen to another antimicrobial regimen either regarding specific molecules, classes of antimicrobials, route of administration, or duration of therapy and the beneficial effects of the 2 regimens were similar, the undesirable outcomes were ranked as critical for decision-making, although several other considerations might also have been taken into account such as stewardship issues and costs.

The suggested interpretation of strong and weak recommendations for patients, clinicians, and healthcare policymakers is listed in Figure 1. The strength of recommendations was established by informal consensus. Feedback was obtained from external peer reviewers. The guideline was endorsed by PIDS. Approximately every 2 years, but more frequently if needed, IDSA will determine the need for revisions to the guideline by an examination of the current literature and the likelihood that any new data will have an impact on the recommendations.

If necessary, the entire expert panel will be reconvened to discuss potential changes. PCR is especially useful when the parasite burden is low; however, blood smear examination is rapid and inexpensive [ 54 , 59 ]. Examination of multiple thin blood smear fields is indicated Figure 5. A review of at least — fields under oil immersion will increase sensitivity, although the number of fields has not been standardized [ 48 ]. Examination of thick blood smears may increase sensitivity because the number of red blood cells examined per field is greater than with thin smears; however, Babesia organisms are small and may be missed on thick blood smears.

Both thick and thin smears should be prepared and examined by experienced personnel, as they can be difficult to interpret. For example, Babesia ring forms can be misinterpreted as Plasmodium falciparum trophozoites. In contrast, merozoites organized in tetrads Maltese cross forms are pathognomonic of babesiosis Figure 5. If blood smears are negative and babesiosis is still suspected, PCR testing should be performed. Babesia microti PCR assays frequently are offered by clinical laboratories, as this species accounts for almost all cases of babesiosis in North America [ 3 ].

Babesia -specific antibody testing should not be used for routine diagnosis of acute babesiosis. Distinguishing active from past infection using serology is difficult because most patients who experience acute babesiosis remain seropositive for a year or more after resolution of disease, despite appropriate antimicrobial therapy [ 29 , 30 , 60 , 61 ]. As with most serologic tests, optimal performance requires analysis of paired serum samples collected during the acute and convalescent phases of illness [ 62 ]. This approach is impractical for the diagnosis of acute babesiosis. Antibody testing is used to determine the seroprevalence of Babesia infection in epidemiological studies and may have a role in screening the blood supply [ 20 , 29 , 30 , 63 ]. Symptomatic patients who test positive for Babesia non- B.

The whole cell B. Sera from B. Early diagnosis of symptomatic patients hastens appropriate antimicrobial therapy, which typically reduces the severity and duration of symptoms and helps prevent complications [ 37 ]. A diagnosis of babesiosis should be considered for any patient who presents with typical symptoms especially fever, fatigue, chills, sweats, headache, and anorexia , characteristic routine laboratory test abnormalities, and who lives in, or has traveled to a Babesia endemic region within the previous month or who has received a blood transfusion within the previous 6 months. Most patients who acquire babesiosis through blood transfusion develop symptoms after a 1 to 9 week incubation period but it can be can as long as 6 months [ 27 ].

Borellia burgdorferi infection is more common than B. Based on a limited number of studies in areas where both B. Lyme disease patients coinfected with B. Babesiosis coinfection should be considered in Lyme disease patients with severe illness, in those whose symptoms are unlikely to be explained by B. The pretest probability of babesiosis in a person who does not live in or has not traveled to an endemic area within the previous month is low, and testing for Babesia in such individuals is not warranted.

Confirmation of the diagnosis requires identification of intraerythrocytic Babesia parasites on blood smear or amplification of Babesia DNA in blood using molecular methods such as PCR. In patients with symptomatic babesiosis, parasitemia usually is high enough that blood smear examination and PCR perform similarly. Additional studies are needed to assess whether CBC, liver enzymes, and markers of hemolysis are clinically useful for screening patients prior to ordering laboratory testing specific for babesiosis.

Additional studies also are needed to determine whether blood smear or PCR should be the initial test used to diagnose acute babesiosis and monitor patients during therapy. More rapid, sensitive, specific, and cost-effective diagnostic tests are being developed but require clinical validation [ 52 , 53 , 55 , 73—77 ]. Comment: A single positive antibody test is not sufficient to establish a diagnosis of babesiosis because Babesia antibodies can persist in blood for a year or more following apparent clearance of infection, with or without treatment.

The IFA test is routinely used to detect B. The B. A single positive Babesia antibody test result cannot reliably distinguish between an active and a resolved Babesia infection because Babesia antibodies can persist for more than a year following apparent clearance of infection, with or without treatment [ 29 , 30 , 60 , 79 ]. Antibiotic treatment also incurs the risk of side effects, as well as additional costs. The duration of treatment is 7 to 10 days in immunocompetent patients but often is extended when the patient is immunocompromised Table 1. In a prospective, nonblinded, randomized trial in immunocompetent patients with non life-threatening babesiosis due to B.

All medications were prescribed orally for a 7-day treatment course. Based on time to resolution of symptoms, the 2 regimens had comparable efficacy. Persistent symptoms were severe enough in 4 of 18 patients given clindamycin plus quinine that they required hospital admission after 1—2 days of treatment compared with none of 40 patients given atovaquone plus azithromycin. In a subsequent retrospective study of 40 patients hospitalized because of severe babesiosis and treated exclusively with atovaquone plus azithromycin, including 11 patients who had life-threatening disease, the combination of atovaquone plus azithromycin was found to be well-tolerated and effective [ 39 ]. In some instances, the diagnosis of babesiosis is made after acute illness has resolved.

Asymptomatic patients do not require antimicrobial therapy unless parasites are seen on thin blood smear for more than a month. Numerous immunodeficiencies and comorbidities have been associated with severe babesiosis, including asplenia and hyposplenism, cancer, congestive heart failure, HIV infection, immunosuppressive drugs, and advanced age. Neonates may experience severe babesiosis after transfusion of B.

The severity of babesiosis differs among these disease categories [ 3 , 28 , 31 , 33 , 37 ]. Some immunocompromised patients experiencing babesiosis require more intense therapy for longer duration than immunocompetent patients. A subgroup of highly immunocompromised patients reported in a case-control study required at least 6 consecutive weeks of antibiotic therapy, including 2 final weeks during which parasites were no longer detected on peripheral blood smear [ 28 ].

Eleven of 14 patients had B cell lymphoma or another malignancy, of whom 8 were also asplenic, and 7 had been treated with rituximab. The duration of treatment was noted to be more important than the antibiotic combination used to achieve a cure [ 28 ]. Therapeutic failure in these cases was attributed to amino acid substitutions in the regions of B. A small number of B. Most were treated with IV clindamycin plus oral quinine for 7—10 days [ 7 , 8 , 19 , 83 , 84 ].

The efficacy of atovaquone plus azithromycin in treating such infection has not been evaluated. To date, more than 50 cases have been reported. Almost all B. These patients usually are treated with IV clindamycin plus oral quinine. Cats with regressive infection appear to have the same life expectancy as cats that have never been exposed to FeLV. The typical clinical signs of FeLV infection usually develop in cats with progressive infection, often not until after several years of viraemia Hardy et al. Experimentally, susceptible kittens can be protected from FeLV infection following passive immunisation with high titred antisera against FeLV Hoover et al.

This observation suggests that antibodies have a role in providing protection. However, once progressive infection has become established, this treatment is ineffective Weijer et al. Most cats that overcome FeLV viraemia exhibit high virus neutralising antibody titres Russel and Jarrett, ; Lutz et al. In most - but not all - cats that overcame viraemia, virus neutralising antibodies can be detected Flynn et al. Since not all immune cats develop high antibody titres, it was concluded that cytotoxic T-lymphocytes CTLs are also important in FeLV immunity Lutz et al. Antibody development was observed in some cats as the sole evidence of FeLV infection Major et al.

Since some of them developed antibodies, it was concluded that the virus had replicated somewhere to sufficient levels to trigger antibody synthesis. The observation that PCR analysis of several organs was negative indicates that further replication must have been controlled by the immune system. FeLV infections can cause variable and multiple clinical signs. The most common disease consequences of progressive FeLV infection are: immune suppression, bone marrow suppression, and lymphoma Hardy et al.

The prognosis for cats with progressive FeLV infection is poor, and most will develop clinical signs typical for this infection. Some progressively infected cats may remain healthy for years before an FeLV-related disease develops, and occasionally some enjoy lifelong health Hofmann-Lehmann et al. Viral and host factors, like the virus subgroup and the cell-mediated immune response, influence the pathogenesis in individual cats. Immune suppression in FeLV infected cats is more complex and severe than the more selective one caused by feline immunodeficiency virus FIV infection. Whether clinical signs are present or not, every cat with progressive FeLV infection is immune-suppressed Perryman et al.

The immune suppression may have diverse clinical consequences and may allow infection with agents to which cats would be normally resistant, such as mycobacterial infections. In addition, there may be exacerbation of disease caused by other pathogens, such as poxvirus, haemotropic mycoplasmas and Cryptococcus species, and of infections normally not pathogenic in cats, e. Concurrent FeLV infection may also predispose to chronic refractory disease, such as stomatitis and chronic rhinitis Knowles et al.

Chronic rhinitis and subcutaneous abscesses may take much longer to resolve in progressively FeLV-infected cats, and unexpected recurrences may arise. FeLV-infected cats may develop many different types of anaemia Fig. Regenerative anaemias, associated with haemolysis may be related to secondary opportunistic infections, for example by Mycoplasma haemofelis , or to immune-mediated destruction of red blood cells Scott et al. Non-regenerative anaemias may be caused by the direct bone marrow suppressive effects of the virus, chronic inflammatory mechanisms, or myeloproliferative disease.

Other cytopenias may be present, e. FeLV may cause different tumours in cats, mainly lymphoma and leukaemia, but also other non-haematopoietic malignancies. Lymphomas are among the most frequent tumours of the cat and are sometimes caused by FeLV infection Francis et al. However, it should be noted that today the vast majority of lymphomas are not associated with FeLV. Different forms of lymphoma have been classified according to their most frequent anatomic location:. In some cases, lymphoma is disseminated with multiple organ and site involvement Hardy et al. Different types of acute or chronic leukaemia have been described depending on the neoplastic transformed cell type.

Multiple fibrosarcomas in young viraemic cats have occasionally been associated with infection with FeSV feline sarcoma virus , a recombinant virus developing from recombination of the FeLV-A genome with cellular oncogenes Hardy, ; Donner et al. Benign peripheral lymphadenopathy has been diagnosed in FeLV-infected cats Moore et al. Chronic enteritis associated with degeneration of intestinal epithelial cells and crypt necrosis has been associated with FeLV-infection in cats in which virus was present in intestinal crypt cells Reinacher, Inflammatory and degenerative liver disease has also been described in association with FeLV infection Reinacher, Neuropathogenicity has been considered as a possible direct effect of the virus Dow and Hoover, Immune-mediated diseases associated to FeLV infection have been reported, including immune-mediated haemolytic anaemia, glomerulonephritis, uveitis and polyarthritis.

Antigen-antibody complex deposition and loss of T-suppressor activity may be the main factors contributing to immune-mediated diseases. Reproductive disorders and fading kitten syndrome have been also reported. Foetal resorption, abortion and neonatal death are the main manifestations Hardy, Fading kittens and reproductive disorders are rarely observed today, largely as a result of the very low prevalence of infection in pedigree breeding cats.

Such tests had the advantage of allowing quantitation of p27 but had a tendency to produce false-positive results as the antibodies did not only detect viral proteins but occasionally also non-viral components Lutz et al. This assay utilises a single monoclonal antibody specific for an epitope A of p27 fixed to a solid phase. The serum sample to be tested is mixed with one or two additional monoclonal antibodies specific for epitopes B and C of p27, and the mixture is then added to the solid phase.

Hence the presence of p27 leads to insolubilisation of the enzyme-conjugated antibodies and the resulting colour change is indicative for the presence of p27, a marker of progressive infection or of transient viremia in some cats with the regressive form of infection during the early phase. ELISA procedures have the advantage of high diagnostic sensitivity and specificity. These tests are based on the same principle as the ELISA but small beads less than one micron in size are coated to the revealing antibodies rather than enzymes.

The diagnostic sensitivity and specificity of immune chromatography tests was shown to be comparable to those of the ELISA Robinson et al. The first method that allowed FeLV detection in progressively infected cats under field conditions was the indirect IFA, introduced in Hardy et al. It was based on the observation that granulocytes, lymphocytes, and platelets in progressively infected cats contain gag components, which may be detected by IFA in blood smears.

Thus, it becomes positive later than the ELISA and only in the phase of the second viraemia, when bone marrow cells are infected. If a progressively infected cat has leukopenia or if only a small percentage of peripheral leukocytes are infected, the presence of FeLV infection may be overlooked using IFA tests. Furthermore, all eosinophils have a tendency to bind the FITC conjugates used for IFA resulting in false positive tests if slides are not read carefully Floyd et al. Virus isolation in cell culture has been considered to be the ultimate criterion for progressive FeLV infection Jarrett, ; Jarrett et al. Since every cat cell carries between 12 and 15 copies of endogenous FeLV, it was difficult to determine sequences specific for detecting exogenous provirus in early research Jackson et al.

The value of PCR techniques was greatly enhanced by the development of highly specific real-time PCR assays that not only allow detection but also quantitation of exogenous FeLV provirus Hofmann-Lehmann et al. PCR for the detection of provirus in whole blood can be useful for the clarification of inconclusive p27 antigen tests. Moreover, PCR from whole blood may be helpful in the very early phase of infection. And finally, it may be applied in catteries to confirm absence of FeLV or identify regressively infected cats provirus carriers and it may be useful to investigate cats with clinical signs that may be FeLV-associated but that are antigen-negative.

This technique permits the detection and quantitation of viral genetic sequences in the absence of cells. Many cats that have overcome FeLV viraemia remain provirus-positive regressively infected but do not have detectable viral RNA in plasma, saliva or faeces Gomes-Keller et al. The use of saliva as the substrate represents an alternative for assessing the infectious state of a cat without leading to unnecessary stress to the patient which usually resents blood sampling.

Moreover, the sample collection does not require trained personnel. RT-PCR from plasma and saliva may also be helpful in the very early phase of infection. In most situations, individual cats are tested for FeLV infection. However, when the cost of testing is a limitation, pooled saliva samples can be used for RT-PCR, as the assay is sufficiently sensitive to detect a single infected cat in a pool of up to 30 samples. This approach may be chosen when screening multi-cat households Gomes-Keller et al. The observation that antibodies can develop as the sole parameter of exposure to FeLV Major et al.

In contrast to published results Fontenot et al. Although antibodies against various FeLV components can be measured, the results are difficult to interpret because some cats develop antibodies to their endogenous FeLV. Therefore, such tests are currently of little clinical value, with the possible exception of p15E Boenzli et al. Virus-neutralising antibodies can be measured, but this test is not widely available except in the UK and is used infrequently. In some research laboratories, the so-called FOCMA feline oncornavirus-associated cell membrane antigen test was used to detect antibodies to what was believed to be a tumour-associated antigen.

As this test is difficult to establish and to standardise, it is not considered to be of clinical value. Cats with progressive infection are usually positive in all those tests. As the prevalence of FeLV infection has decreased in many European countries, also the percentage of false positive test results tend to increase. Therefore, a positive result in a healthy cat should always be confirmed, preferably using provirus PCR offered by a reliable laboratory. A positive ELISA or immunochromatography result in a cat with clinical signs consistent with FeLV infection is more reliable, as in sick cats the prevalence of FeLV is considerably higher, and the higher the prevalence the higher the probability of a test to be correctly positive.

Cats in which an antigen-positive test result has been confirmed can overcome viraemia regressive infection after weeks, usually by twelve weeks — in rare cases even later; in one documented case more than a year after infection Hofmann-Lehmann et al. Therefore, every antigen-test-positive healthy cat should be separated and retested after 6 or more weeks; if the cat still tests antigen-positive retesting can be repeated. These cats should be considered regressively infected.

The clinical relevance of regressive infection has not been fully established; in some instances, immune suppression or infection with other viruses may lead to reactivation. The mean proviral load in cats with regressive infection is several hundred times lower than in cats with progressive infection once the infection has fully established several weeks after infection. These cats have foci of infection outside the bone marrow from which soluble p27 is released into the circulation; such cats are potential sources of infection Lutz et al.

Progressively FeLV-infected cats should be strictly confined indoors, to prevent spread to other cats in the neighbourhood. There may also be benefits in preventing exposure of the immune-suppressed retrovirus-infected cat to infectious agents carried by other animals. This is true for the home environment as well as for the veterinary hospital. Although they can be housed in the same ward as other hospitalised patients, they should be kept in individual cages. Since they may be immune-suppressed, they should be kept separated from cats with other infectious diseases. Management should be aimed at minimising potential exposure to other infectious agents.

In addition to confining the cat indoors it may be prudent to avoid feeding uncooked meat, which may pose a risk of bacterial or parasitic infections to which progressively infected cats are more susceptible. Asymptomatic FeLV-infected cats should receive clinical check-ups at least every six months. A complete blood count CBC , biochemistry profiles and urinalyses should be performed periodically, ideally every six to twelve months. Intact male and female FeLV-infected cats should be neutered to minimise the risk of virus transmission and for health benefits.

Surgery is generally well tolerated by asymptomatic FeLV-infected cats. The virus is infectious only for a short while outside the host Francis et al. Vaccination programmes to prevent common infectious diseases should be maintained in such cats, although they may not mount an adequate immune response to, e. Therefore, protection of a progressively FeLV-infected cat may not be as good as that of an uninfected animal. If these cats are allowed outside — which is not recommended — more frequent vaccination may be considered. Inactivated vaccines are recommended whenever available, because it cannot be excluded that modified live virus vaccines may be able to cause symptoms in immune-suppressed cats.

If FeLV-infected cats are sick, prompt and accurate diagnosis of associated or secondary conditions is important to allow early therapeutic intervention and successful treatment. Therefore, more intensive testing should be implemented earlier in the course of illness than in uninfected cats. Many cats with FeLV infection respond well to appropriate medications although a longer or more aggressive course of therapy e. Corticosteroids, other immune-suppressive or bone marrow-suppressive drugs should generally be avoided, unless used as a treatment of FeLV-associated malignancies or immune-mediated disease. If chronic gingivostomatitis is present, glucocorticoids should not be used, with except in extreme circumstances.

In cats with gingivostomatitis, full mouth extraction is preferred over the use of glucocorticoids. Many complications of FeLV infection respond well to treatment, such as secondary bacterial infections, especially with Mycoplasma haemofelis , which often improves with antibiotic treatment, e. Treatment regimes for lymphomas, particularly based on chemotherapeutic drugs, are well established, and the same protocols should be applied to cats with lymphoma that are FeLV-infected. The results of studies on FeLV as a negative prognostic factor with regard to remission and survival times in lymphoma patients are contradictory Mooney et al.

In a recent study, FeLV antigen-negative cats with lymphoma had significantly longer remission times days than FeLV antigen-positive cats 25 days when both groups received anti-tumour chemotherapy Meichner et al. In another study, the median remission and survival times for FeLV antigen-positive cats were 27 and 37 days and for FeLV antigen-negative cats, and days Vail et al. The prognosis of lymphoma in cats with progressive FeLV infection is poor because of bone marrow suppression, which is usually exacerbated by chemotherapy and can frequently delay treatment.

Immunosuppression caused by FeLV infection also is aggravated by chemotherapy, leading to secondary infection that may cause overt clinical signs and impair quality of life. Furthermore, FeLV-associated lymphomas are associated with a higher rate of mitoses Valli et al. The prognosis is also guarded because of the theoretical risk of development of additional lymphoid malignancies in cats with FeLV-associated lymphoma. During virus replication, FeLV is integrated into the host genome and recombination with endogenous FeLV-related sequences could form new and more pathogenic variants, such as FeLV subtype B, with the potential of new lymphoma formation at any time.

Finally, owners of cats with progressive FeLV infection and lymphoma often elect euthanasia and do not comply with treatment. There is little evidence from controlled studies to support the efficacy of immune modulators on the health or longevity of FeLV-infected cats. Nevertheless, it has been suggested that some of these agents may benefit infected animals by restoring compromised immune function, thereby allowing the patient to control its viral burden and recover. Although uncontrolled studies have suggested dramatic clinical improvement e. Staphylococcus Protein A is a bacterial polypeptide purified from cell walls of Staphylococcus aureus Cowan I that acts as an immune modulator.

The efficacy of antiviral drugs is limited, and many cause severe side effects Hartmann, Only a few controlled studies have demonstrated some effect of a few drugs in FeLV infected cats see tables 1, 2 and 3. Treatment of FeLV-infected cats with anaemia Give blood transfusions if anaemia is severe. Table 2: Summary on studies on efficacy of antiviral drugs for treatment of feline leukaemia virus infection including EBM grades for judgment of the available efficacy data including expert opinion of the authors.

References : 1 Tavares et al. Table 3: Summary on studies on efficacy of immunomodulatory drugs for treatment of feline leukaemia virus infection including EBM grades for judgment of the available efficacy data including expert opinion of the authors. References : 20 Jameson and Essex, ; 8 Stuetzer et al. Treatment of FeLV-viraemic cats significantly improved their health and extended their survival time, but it did not resolve viraemia De Mari et al.

No viral parameters, however, were measured to support the assumption that interferon exerted an anti-FeLV effect rather than inhibited secondary infections. The drug effectively inhibits FeLV replication in vitro , and in vivo in experimental infections. It can reduce plasma virus load, improve the immunological and clinical status, increase the quality of life, and prolong life expectancy in FeLV-infected cats.

Higher doses should be used carefully, as side effects e. The drug is tolerated very well by cats and within one week leads to a marked reduction in viral loads. However, this reduction is not sufficient for the immune system to control the viraemia, and treatment has to be continued over long periods in order to maintain low viral loads and prevent disease Boesch et al. After several experimental vaccines had been described Jarrett et al. It was based on conventionally prepared FeLV antigens, and it protected cats from viraemia Lewis et al. A number of FeLV vaccines are now available in Europe. Some used recombinant DNA technology, like the one consisting of the viral envelope glycoprotein as well as part of the transmembrane protein expressed in E.

The avian Babesia species are characterized as having ring and amoeboid forms, and fan-shaped or cruciform cross-shaped tetrad schizonts. Developing parasites have only been reported in red blood cells. For centuries, the animal disease was known to be a serious illness for wild and domesticated animals, especially cattle. He documented the disease by describing signs of a severe hemolytic illness seen uniquely in cattle and sheep. They also identified the tick as the transmitting agent, a discovery which first introduced the concept of arthropods functioning as disease vectors. It was believed to be a disease that only affected nonhuman mammals, but in , the first case of babesiosis was seen in a human. This proved the parasite was a potential pathogen in anyone.

Babesia show host specificity , allowing many different subspecies of Babesia to emerge, each infecting a different kind of vertebrate organism. In different environments, individual protozoa may develop mutations which, when they increase the protozoa's fitness , allow the population to increase their numbers. This specificity explains why Babesia have such great genetic diversity.

Babesia selfishly persists long-term in the host's system: the host gains no benefit from the parasite invasion and only suffers. This allows the parasite to exploit all resources offered by the host, to increase in number, and to increase the rate of transmission. Infection typically stimulates the innate immune system , and not the humoral immune system. The genome of B.

Partial RNA sequencing of canine piroplasms has identified a number of additional species. The life cycle of B. It is transmitted by ticks of the family Ixodidae between these hosts. To begin, the tick as the definitive host becomes infected itself, as it takes up gametocytes when attached for a blood meal. It also introduces the Babesia into the intermediate host e. As Babesia enter the animal's red blood cells erythrocytes , they are called sporozoites. Within the red blood cell, the protozoa become cyclical and develop into a trophozoite ring. The trophozoites moult into merozoites , which have a tetrad structure coined a Maltese-cross form.

The gametes are fertilized in the tick gut and develop into sporozoites in the salivary glands. These are the sporozoites the infected tick introduces when it bites an intermediate host. Even as an incidental host , the phase changes which occur in the parasite are the same within humans as in the biological hosts. Babesia can be diagnosed at the trophozoite stage, and can also be transmitted from human to human through the tick vector, through blood transfusions, or through congenital transmission an infected mother to her baby. Cold weather completely interrupts transmission. High humidity and rainfall accommodate ticks carrying Babesia.

Babesia species are spread through the saliva of a tick when it bites. Already at its nymphal stage, a tick bites into the skin for a blood meal. The tick, if not removed, stays attached for three to four days, with longer periods of feeding associated with a higher probability of acquiring the parasite. The parasite can survive in the tick as it molts through its various developmental stages, resulting in all tick stages being potentially infectious. Some species of Babesia can be transmitted from a female tick to its offspring before migrating to salivary glands for feeding.

Ticks of domestic animals that transmit Babesia and cause much disease include the very widespread cattle ticks, Rhipicephalus Boophilus microplus , and R. These ticks have a strict one-host feeding cycle on cattle, so the Babesia can only be transmitted by the transovarial route. In the Americas, Ixodes scapularis is the most common vector. This hard tick, commonly known as a deer tick, is also the vector for other tick-associated illnesses, such as Lyme disease.

Many species of Babesia only infect nonhuman mammalian hosts, most commonly cattle, horses, and sheep. Their reservoirs are theorized to be the white-footed mouse Peromyscus leucopus , voles from the Microtus genus , and the white-tailed deer Odocoileus virginianus. Most cases of transmission between humans are attributed to a tick vector. As of , the Centers for Disease Control and Prevention CDC acknowledged more than 40 cases of babesiosis contracted from transfusions of packed red blood cells PRBC , as well as two infections documented from organ transplantation. PRBC transfusions that cause infections were identified through testing the blood donor for B. Transmission is also possible through congenital transmission from an infected mother to her baby.

As symptoms may not appear, many women may not be aware they are infected during pregnancy, and therefore a measurement of congenital transmission rate is not known at this time. Currently, no vectors for avian Babesia have been identified, but they are assumed to be ticks. Of the species to infect humans, B. Endemic areas are regions of tick habitat, including the forest regions of the northeastern United States and temperate regions of Europe. For reasons that remain unclear, in areas endemic to both Lyme disease and babesiosis, Lyme disease transmission prevails and is more predominant in the region. There are 15 avian species of Babesia, and four Babesia have been reported from sea hosts.

About 40 cases of human babesiosis, caused by intraerythrocytic protozoans protozoa inside red blood cells of the genus Babesia , were reported in Europe. Bovine babesiosis caused by B. Signs of infection with B. In other cases, symptoms are characterized by irregular fevers, chills, headaches, general lethargy, pain, and malaise. Splenectomized patients are more susceptible to contracting the disease and can die within five to eight days of symptom onset. Complications include acute respiratory failure , congestive heart failure , and kidney failure. Infected individuals suffer from hemoglobinuria followed by jaundice, a persistently high fever, chills, and sweats. If left untreated, B. The pathogenicity of B. Birds were found with lesions , anemia and respiratory difficulty, and tissues of avian hosts were affected.

As a protozoan parasite, the most effective way to identify Babesia infection is through blood sample testing. Babesia species enter red blood cells erythrocytes at the sporozoite stage.

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