Postweaning Multisystemic Wasting Syndrome Induced after Experimental Inoculation of Cesarean-Derived, Colostrum-Deprived Piglets with Type 2 Porcine Circovirus

Abstract

Cesarean-derived, colostrum-deprived pigs (n = 23) were inoculated intranasally and subcutaneously with a low cell culture passage of type 2 porcine circovirus. In 11 pigs, a persistent fever that lasted 7-17 days began 12-15 days after inoculation with virus. Additional signs of disease in those 11 pigs included depression (11 of 11 pigs), palpable enlargement of inguinal, prefemoral, and popliteal lymph nodes (11 of 11), icterus (6 of 11), and hyperpnea (2 of 11). The remaining 12 pigs had fever that occurred intermittently for 2-4 days between days 12 and 20 postinoculation. Overt signs of disease in those pigs were limited to palpable enlargement of inguinal and popliteal lymph nodes (9 of 12 pigs). When compared with control pigs of similar age, the average daily rate of weight gain for all pigs inoculated with virus was less over a 2-week period that began 2 weeks post inoculation. At postmortem examination, lymph node enlargement was seen in 14 of 14 pigs euthanized between days 20 and 28 postinoculation. Lymph node enlargement was especially prominent in pigs that developed a persistent fever. Microscopic lesions noted in pigs that developed a persistent fever included cellular depletion in lymphoid tissues; hepatic cell necrosis; and lymphogranulomatous inflammation of lymph nodes, Peyer's patches of the intestine, liver, kidney, and heart. Virus was isolated with varying frequency from nasal, rectal, or tonsil swab specimens, buffy coat, serum, urine, and lung lavage fluid obtained antemortem or postmortem. Virus was isolated from or viral DNA was detected in a variety of tissues obtained postmortem up to 125 days postinoculation. Antibody against type 2 porcine circovirus usually was detected in serum between 15 and 20 days postinoculation; however, antibody against virus was not detected in serum from 4 pigs euthanized 20-24 days postinoculation. Direct contact with pigs inoculated with virus 42 days previously resulted in transmission of virus to 3 of 3 control pigs.

Lack of an effect of a commercial vaccine adjuvant on the development of postweaning multisystemic wasting syndrome (PMWS) in porcine circovirus type�2 (PCV2) experimentally infected conventional pigs

“…The serological profile observed in both PCV2 inoculated groups was similar, and was in agreement with those from other experimental trials, with an increase of antibody titres occurring after 2 weeks PI, shortly after viremia detection [7,17,19]. Viremia coexisted with high antibody titres until the end of the experiment, which suggests that PCV2 can evade a specific immune response, or alternatively, an effective immune response was of slow development, as suggested by other authors [22].…”

“…No characteristic PMWS lesions [8,23] were found at the experimental termination day, despite the occasional presence of the viral genome in some lymphoid tissues. The only clinical evidence of the viral infection was an intermittent hyperthermia, between days 16 and 19 PI, which coincided with the onset of viremia and the highest viral load in the serum, which is in concordance with the results from other PCV2 experimental trials [7,24].…”

“…The genome consists of a singlestranded molecule of circular DNA [18,25]. PCV2 is recognised as the cause of a clinical condition of swine named postweaning multisystemic wasting syndrome (PMWS) [2,7,9]. This disease mainly affects 5 to 12 week-old pigs, and is clinically characterised by growth retardation, skin pallor, dyspnea, and enlargement of the inguinal lymph nodes.…”

“…Main gross findings include non-collapsed lungs, and generalised lymphadenopathy. Histological characteristic lesions of PMWS consist of lymphocyte depletion and histiocytic infiltration, often with multinucleate giant cells and amphophilic intracytoplasmatic inclusion bodies in lymphoid tissues [7,23]. Histological lesions are systematically associated with PCV2 antigen and/or nucleic acid [23].…”

“…Koch postulates have been fulfilled for PCV2 as the primary cause of PMWS [2,7,10]. However, the severe clinical expression observed in field cases has been difficult to reproduce experimentally [1], suggesting that the disease is probably of multifactorial aetiology and/or that not all hosts are susceptible to the development of the disease.…”