Akabane virus infection presents a complex challenge in livestock management, demanding accurate and timely diagnosis for effective herd management. The clinical manifestations and pathological impacts of Akabane virus are significantly influenced by the animal species affected and, critically, the gestational stage at the time of infection. In cattle herds with year-round calving, veterinarians may encounter a spectrum of abnormalities, highlighting the importance of comprehensive Akabane Diagnosis. The most severe congenital defects arise when susceptible cows are infected between approximately 80 to 150 days of gestation, though susceptibility extends beyond this window, affecting calves at various stages after the initial two months of pregnancy.
Late gestational Akabane virus infections in calves can result in live births, but with debilitating conditions. These calves may exhibit an inability to stand and display flaccid limb paralysis or incoordination, presenting immediate diagnostic clues. Infections occurring earlier in gestation, specifically between 120 to 180 days, often lead to rigid limb fixation, typically in flexion, known as arthrogryposis. Furthermore, conditions like torticollis, kyphosis, and scoliosis may also be observed, complicating Akabane diagnosis and often leading to dystocia and severe obstetric issues. These complications can unfortunately result in reduced fertility and even mortality in cows, underscoring the economic and animal welfare implications of Akabane virus.
The progression of arthrogryposis severity in newborn calves offers a diagnostic timeline. Calves born initially with arthrogryposis tend to be less severely affected compared to those born in the subsequent 4 to 6 weeks. Early cases might only show involvement in one or two joints of a single limb. However, later cases can present with severe fixation across multiple joints and limbs, emphasizing the evolving nature of the outbreak and the need for ongoing Akabane diagnosis and monitoring within a herd. Calves infected between 80 and 120 days of gestation, while often born alive, may exhibit poor mobility, depression, and blindness. These symptoms are directly linked to porencephaly or hydranencephaly, critical pathological findings in Akabane diagnosis. In severe hydranencephaly cases, mid-gestation abortions can occur, further complicating herd management and highlighting the diverse clinical presentations of Akabane virus.
Less frequently, certain Akabane virus strains can induce disease in calves infected in the early weeks of life. This manifests as a range of neurological signs and pathology consistent with acute viral encephalitis. Notably, in Japan, strains causing disease in adult cattle have also been documented, broadening the spectrum of Akabane virus impact beyond congenital abnormalities and highlighting the need for vigilance in Akabane diagnosis across different age groups.
In small ruminants, concurrent lesions of arthrogryposis and hydranencephaly are frequently observed, often within the same animal, which is a crucial diagnostic indicator in these species. Lambs and kids infected with Akabane virus can also exhibit pulmonary hypoplasia and spinal cord hypoplasia, expanding the range of potential defects. The majority of Akabane-infected lambs and kids are stillborn or perish shortly after birth, with abortions also being a common outcome, emphasizing the severe impact of the virus on small ruminant populations and the importance of accurate Akabane diagnosis for flock management.
While suspected in horses, Akabane virus-induced congenital abnormalities, particularly arthrogryposis and hydranencephaly, have lacked definitive laboratory confirmation. This highlights a gap in current Akabane diagnosis capabilities and the need for further research in equine populations.
Similar clinical signs to Akabane virus infections in ruminants are also observed with Schmallenberg, Shamonda, and Aino viruses, all belonging to the Simbu serogroup of orthobunyaviruses. Typically, the incidence of disease is lower with these related viruses unless infection occurs in intensively managed breeding programs employing rigorous synchronization. Such programs can lead to a large number of animals at similar pregnancy stages, increasing vulnerability to outbreaks and necessitating careful differential Akabane diagnosis. When Schmallenberg virus initially emerged in Europe, adult animals experienced a mild febrile illness with diarrhea, a symptom not subsequently observed, indicating the evolving clinical picture of these related viral infections and the importance of ongoing surveillance and refined diagnostic approaches.
Shuni virus, another member of the Simbu serogroup found in Africa, has been identified as a cause of acute encephalitis in horses, further broadening the differential Akabane diagnosis considerations in equine neurological diseases. Shuni virus has also been linked to congenital defects in cattle in Israel and has caused severe, fatal encephalitis in calves, demonstrating the widespread impact and diverse clinical presentations of viruses within the Simbu serogroup and the necessity for comprehensive diagnostic strategies.
Lesions in Akabane Diagnosis
Histological examination of calves infected late in gestation with Akabane virus may reveal disseminated encephalomyelitis, a key pathological lesion for Akabane diagnosis. Neurogenic muscle atrophy, resulting from spinal motor neuron loss, is observed histologically in calves infected between 120 and 180 days of gestation. These lesions are directly responsible for the varying degrees of arthrogryposis, torticollis, kyphosis, and scoliosis observed clinically, making them crucial factors in understanding the pathogenesis and refining diagnostic approaches.
In calves infected between 80 and 120 days of gestation, brain examination often reveals varying degrees of cerebral hemisphere cavitation, ranging from porencephaly to severe hydranencephaly. In extreme cases, hydranencephaly can lead to the near-total destruction of cerebral hemispheres, leaving only the brain stem intact. These severe lesions are more prevalent in animals infected during earlier pregnancy stages. The stark contrast between the severity of these gross lesions and the clinical state of affected calves underscores the subtle yet profound neurological damage caused by Akabane virus, highlighting the importance of detailed pathological examination in Akabane diagnosis.
A critical differential diagnostic feature for Akabane virus infection is the near absence of gross or histologic lesions in the cerebellum. This is a valuable distinguishing factor from other teratogenic viruses such as bovine viral diarrhea virus (BVDV). While BVDV often presents with cerebellar lesions, their absence in conjunction with cerebral lesions strongly suggests Akabane virus infection. However, it’s important to note that other Simbu serogroup viruses may produce lesions throughout the brain, necessitating a broader differential diagnosis and potentially advanced diagnostic techniques for definitive identification.
Akabane or Schmallenberg virus infections in fetal sheep and goats induce a range of gross and histologic lesions similar to those in cattle. However, a greater diversity and severity of pathology can be observed within the same animal, likely due to the shorter gestation period in these species. This variability emphasizes the need for careful and comprehensive pathological examination in Akabane diagnosis across different ruminant species to accurately assess the full spectrum of disease manifestations.
