Congenital anaplasmosis in a newborn calf from southern Brazil

Background: Bovine anaplasmosis is a hemolytic disease caused by Anaplasma marginale, which is transmitted mainly by ticks and less frequently by hematophagous insects or contaminated fomites. Although adult cattle are most affected, neonatal infections may occur when transplacental dissemination occurs during late gestation. Congenital anaplasmosis is rarely reported in South America and may be overlooked because its clinical presentation overlaps with that of other neonatal icteric syndromes. This case report describes the clinical, pathological, and cytological features of congenital anaplasmosis in a newborn calf from southern Brazil.Case: A 2-day-old Jersey calf with marked jaundice, lethargy, and weakness since birth was submitted for necropsy examination. According to the owner, 2 other calves had died between 1 and 2 days of life with similar signs of illness. Gross examination revealed generalized icterus involving the mucosa, subcutaneous tissue, and serous membranes, splenomegaly with red pulp protrusion, and a friable, brick-colored liver. Tissue samples were fixed in 10% buffered formalin and processed routinely for histology, and liver and spleen imprints were stained using a rapid panoptic stain. Microscopically,the liver exhibited multifocal centrilobular necrosis with mild mononuclear infiltrates, the spleen showed congestion and architectural disruption, and the kidneys presented tubular necrosis with mild inflammatory infiltrates. Cytological preparations of the liver and spleen demonstrated basophilic marginal inclusions within erythrocytes, which is consistent with A. marginale. The absence of tick exposure, controlled peripartum management, and immediate onset of clinical signs strongly suggest congenital transmission.Discussion: The gross and microscopic findings were characteristic of acute hemolytic disease and aligned with those reported for neonatal anaplasmosis. Centrilobular hepatic necrosis likely resulted from hypoxia secondary to severe hemolysis, while renal tubular injury may have been caused by hypoxia or pigment-induced nephrotoxicity due to bilirubin and free hemoglobin accumulation. Splenic congestion and architectural loss reflected the intense phagocytic response associated with erythrocyte destruction, a hallmark of the acute phase of A. marginale infection in cattle. Differential diagnoses, such as leptospirosis, septicemia, and neonatal isoerythrolysis, were ruled out based on histopathology and the detection of A. marginale inclusions within erythrocytes in organ imprints. Although congenital transmission is uncommon, it has been documented when maternal infection occurs in late gestation, a period marked by increased placental permeability and heightened susceptibility of the fetus to intrauterine pathogens. The absence of tick exposure, controlled neonatal environment, and immediate onset of clinical signs strongly support vertical transmission in this case. These findings underscore the need to consider congenital anaplasmosis in the differential diagnosis of neonatal jaundice and weakness, especially in endemic regions where adult cattle frequently serve as reservoirs of the disease. Moreover, this case highlights the importance of targeted preventive strategies in pregnant cows, including vector control and monitoring of subclinical infections. From an epidemiological perspective, documenting congenital infection expands our understanding of Anaplasma marginale transmission dynamics and illustrates an alternative route that may influence neonatal morbidity in endemic herds. The results also emphasize the diagnostic value of cytological examination and histopathology in identifying acute infections when molecular testing is unavailable.Keywords: Anaplasma marginale, cattle, neonatal jaundice, transplacental transmission