What clinical signs and laboratory abnormalities are found in dogs infected with Babesia spp.?
The clinical manifestations found during the course of Babesia spp. infections vary, ranging from subclinical infections to multi-organ failure, with a risk of death [87]. While the spectrum of disease may appear daunting, the collection of an extensive history and clinical presentation data backed by laboratory abnormalities should allow the veterinarian to shorten the list of differential diagnoses [4]. The history and common and diverse clinical signs and laboratory abnormalities observed among the Babesia species, the course of several types of Babesia infection, and prognoses are shown in Table 3.
Primary clinical manifestations and prognosis for dogs infected with the different species of Babesia found in Europe [4]
B. canis
B. vogeli
B. gibsoni
B. microti-like sp.
History and features
Young dogs, adult dogs, hunting dogs/sheepdogs (German Shepherd and Komondor) that live outdoors. A greater number of cases is seen in autumn, and spring
Puppies or adult/older dogs with concomitant infectious or non-infectious diseases
Common in fighting dogs (Pit Bull Terrier and Tosa)
Young, adult dogs, guard/hunting dogs that live outdoors
Severity of disease
Moderate to severe
Mild to moderate
Moderate to severe
Moderate to severe
Clinical signs and laboratory abnormalities that differ among Babesia spp.
Petechiae, epistaxis, vomiting, lymphadenomegaly, hypotension, low T3 syndrome, mild to moderate nonregenerative, normochromic, and normocytic anaemia, regenerative anaemia (less common), leukopenia with neutropenia and/or lymphopenia, hypoalbuminemia, elevation of liver enzymes (ALT, AST, ALP), hypokalemia, hyponatremia, and hyperchloremia, hyperlactatemia, hyperphosphatemia, hypertriglyceridemia, hypoglycemia, prerenal and renal azotemia
Regenerative immune-mediated hemolytic anaemia, nonregenerative anaemia, leukocytosis and leukopenia
Lymph node enlargement, enlargement of the spleen, small-bowel diarrhea, weight loss, protein-losing nephropathy, PU/PD, and abdominal effusion. Mild to severe regenerative immune-mediated hemolytic anaemia, neutropenia and leukocytosis. Hypoalbuminemia, azotemia and elevation of liver enzymes (ALT, ALP)
Azotemia, proteinuria, cylindruria and hyperglobulinemia
Course of infection related to disease manifestation
Acute
Acute and chronic
Acute and chronic
Acute and chronic?
Prognosis
Good to poor
Good
Guarded to poor
Guarded to poor
Reference
[84, 89, 106, 131, 162–167]
[84, 106, 162]
[48, 102, 132, 168–171]
[16, 35, 86, 172]
Common clinical signs and laboratory abnormalities among Babesia spp.: Fever, lethargy, anorexia, pale mucous membranes, weakness, bounding pulse, jaundice, pigmenturia, mild to severe thrombocytopenia, mild to severe regenerative anaemia due to hemolysis, bilirubinemia, bilirubinuria, and haemoglobinuria
The wide range of clinical manifestations depends very much on the species of Babesia causing infection and other factors that affect the severity of the disease, including age, splenectomy, immune competence, and concomitant infection or disease [4, 10]. In addition, disease severity has been associated with parasite density in B. rossi infection [88]. However, limited information is available regarding disease severity and parasite density in other Babesia species. In a recent study, parasite density was not different between survivors and non-survivors in dogs infected with B. canis [89]. It is likely that different Babesia spp. might result in different parasitemias due to differences in disease severity, but further studies need to confirm this hypothesis.
Differences in virulence have been described among Babesia species infecting dogs. In general, it is assumed that the least pathogenic large-sized species of Babesia is B. vogeli, at least for adult dogs, and that the most virulent species is B. rossi, which is probably found only in Africa. The pathogenicity of small-sized Babesia spp., such as B. gibsoni and B. microti-like sp., is moderate to severe [4, 10, 90].
There are clinical signs and clinicopathological abnormalities that are common across all Babesia species infecting dogs (Table 3). Frequent clinical signs associated with canine babesiosis are apathy, weakness, anorexia, pale mucous membranes and a poor general condition. All Babesia species can cause fever, enlarged lymph nodes and spleen, anaemia, thrombocytopenia, jaundice and pigmenturia. Although thrombocytopenia, to a varying extent, is frequently detected, the presence of petechiae or ecchymosis is less common. Thrombocytopenia, when present, varies from mild to severe, as does anaemia. Other abnormalities that can be detected include hypoalbuminemia and hyperbilirubinemia [4, 10]. Depending on the infective species and the course of infection, anaemia can be regenerative; nonregenerative anaemia is more typically associated with B. canis [84]. In all species, anaemia is caused by a combination of intravascular and extravascular hemolysis resulting from parasite-caused injury and rupture of red blood cells, the cells’ increased osmotic fragility, and the activity of secondary immune-mediated processes.
Some clinical signs and clinicopathological abnormalities differ among Babesia species infecting dogs (Table 3). Many dogs could present other clinical signs that are not directly related to hemolysis by piroplasms but that demonstrate the involvement of other organs. These complications are especially prevalent following infection by B. rossi. A non-exhaustive list includes weight loss, acute or chronic nephropathy, glomerulonephritis, coagulation disorders (disseminated intravascular coagulation), jaundice from liver disease, immune-mediated hemolysis or thrombocytopenia, hemoconcentration, shock, metabolic and/or respiratory alkalosis, and/or acidosis, gastrointestinal disorders (vomiting or diarrhea), pancreatitis, ascites, ocular lesions (uveitis or blindness), myalgia, rhabdomyolysis and respiratory problems (edema or acute respiratory distress) [91].
It must be noted that many “carrier” dogs with chronic infections will not present with any clinical signs as the result of premunition or concomitant immunity unless their health deteriorates, for example from immunosuppressive treatment, splenectomy, or any other immune-compromised situation (e.g. post-surgical stress or debilitating disease). This phenomenon has been described in Greyhounds infected by B. vogeli and in Pit Bull Terriers infected by B. gibsoni [45, 92]. It results from the inability of the immune system to eliminate the infection, which then establishes itself with more rigour when the immune system is in abatement [4, 10].