The author of this case report was contacted by a pig herd owner due to a sudden onset of peracute/acute mortality in 2-3-week-old suckling piglets the previous day (day 1). Due to Easter holiday, no veterinary diagnostic laboratories were open for submission of samples until one week later.
The herd was a specific pathogen free (SPF) sow herd producing growers, 25-35 kg, for finisher farms. It ran a 5 ½ weeks batch system based on a sow cycle of 22 weeks (116 days gestation 33 days lactation and 5 days from weaning to insemination) with four batches, each batch comprising approximately 100 sows. The farm has one farrowing unit (containing one room) with 98 farrowing pens and one unit for all the weaners and growers. In the case batch, the farrowing room held 83 sows, eight of them were first parity sows, and 920 piglets. All piglets were weaned and moved to the grower unit on day 14.
The herd was self-recruiting and produced its own breeding sows. No pigs from other farms had been introduced to the herd since a depopulation and repopulation of pigs were completed 3 years ago.
SPF-herds in Norway are required to document absence of Actinobacillus pleuropneumonia, Brachyspira hyodysenteria and toxin producing Pasturella multocida. In addition, the commercial Norwegian pig population as a whole has documented freedom from Mycoplasma hyopneumonia, porcine reproductive and respiratory syndrome virus (PRRSV), swine influenza virus (SIV) except the pandemic H1N1 virus, Aujezkys disease, transmissible gastroenteritis virus (TGEV), porcine epidemic diarrhoea (PED) and at that time, porcine respiratory coronavirus (PRCV) through active serosurveillance (13).
Erysipelas, parvo virus and E. coli vaccinations of the sows were performed according to manufacturer’s recommendations. According to herd health records, the farm had low use of antimicrobials, with treatments only initiated on medical indication and administered as individual pig treatments.
The herd was visited by an on-call veterinarian the same day of the call (day 2). It was noted that approximately 30 piglets had died. No piglets showing clinical signs of disease were found. Four piglets were examined post-mortem (PME) on farm with scarce findings and without reaching any conclusions. During the evening and following night, 80 more piglets had died. The next morning (day 3), a new herd visit were organized with the on-call veterinarian and the author. Piglets and sows showing clinical signs of disease were identified.
The clinical evaluation was limited in time due to the extent and peracute nature of the disease. Single piglets in each pen, lied down in sternal recumbency, with a rapid, superficial breathing. Within minutes affected piglets rolled over in lateral recumbency, did not respond to tactile and vocal stimuli and died. Affected piglets were evenly distributed throughout the pens in the farrowing room, however their littermates appeared unaffected and healthy
Four out of 83 lactating sows had rectal temperatures above 40 oC. They had problems rising, ataxia and had excessive and high-pitched vocalisation. One sow died later the same day.
On farm PME were performed on piglets which had died the night before. A preliminary gross pathology status was pale musculature, serosanguinous fluid in the peritoneal cavity and pericardial sac, fine threads of fibrin over the intestines (Figure 1). Some piglets had intestinal haemorrhages and petechial bleedings in the kidneys.
Based on clinical findings and gross pathology bacterial septicaemias or viruses able to induce acute/peracute disease and high mortality was suspected. A presumptive list of differential diagnoses contained Glaesserella parasuis (Glässer’s disease), Erysipelothrix rhusiopathiae (erysipelas), oedema disease caused by beta-hemolytic Shiga toxin 2e -positive Escherichia coli and Streptococcus suis, classical swine fever virus (CSF) and african swine fever virus (ASF).
Contact was made to the Norwegian Food Safety Authority (NFSA) as the competent authority and the national reference laboratory for CSF and ASF , the Norwegian Veterinary Institute (NVI) informing them of the clinical and preliminary gross pathology findings and that notifiable diseases like classical swine fever and african swine fever were on the differential diagnosis list.
On farm PMEs were performed on altogether 15 piglets. Samples for bacteriologic examination were collected and frozen, including 5 heads, 5 livers, 4 lungs, 1 small intestine and kidneys from five piglets. Samples from heart, lung, liver, kidney and brain from three piglets were collected and fixated on formaldehyde for histopathological evaluation.
Additional herd visits, including clinical evaluations, on farm PME and sampling for laboratory examination were performed on day 4, 10 and 20. Three intact dead piglets and formaldehyde fixated samples from heart and lymph nodes from two piglets were collected on day 4. Six fresh livers and spleens were sampled on day 20.
Blood samples from 10, 5 and 11 piglets were collected on day 4, 10 and 20 respectively. The blood was collected in vacutainers containing ethylenediamine tetra-acetic acid (EDTA) as an anticoagulant. A hematologic profile was obtained from a local lab.
Collection of data regarding management routines, biosecurity and environmental factors were performed in on-farm interviews with the workers on the farm.
The piglets died in three rounds with the highest mortality rates during the first three days (Figure 2).
The most consistent gross pathological findings were serous, protein rich fluids in the peritoneal cavity and in the pericardium, fine threads of fibrin covering the abdominal organs, anaemia and swollen livers and spleens, while the histopathological findings were congestion and oedema in many organs, and an increased haemopoietic activity in the livers and spleens. Six and three formalin-fixed lung tissue samples were immunohistochemistry negative for influenza A virus nucleoprotein and porcine circovirus type 2 (PCV2), respectively.
The bacteriologic examination found G. parasuis in 12 out of 14 samples originating from the frozen specimens collected at day 3. G. parasuis was also isolated in 11 out of 12 of the fresh livers and spleens sampled on day 20. Streptococcus sp was isolated in 2 samples and Strept suis serotype 8 and Strept suis in one each, of the frozen samples. In the fresh livers and spleens there were also found Aerococcus sp in 7 out of 12 samples. Two of the G. parasuis isolates from fresh livers and spleens were typed as serotype 9 based on indirect hemagglutination test (IHA) performed at the Innovative Veterinary Diagnostic laboratory (IVD GmgH, Hannover, Germany).
Low blood cell counts, and a low haemoglobin was found in the blood collected on day 4, confirming anaemia.
The interviews revealed that iron paste given to the piglets within the first 24 hours after farrowing was the only routine iron supplementation for piglets on the farm. The automatic regulation of the ventilation system of the farrowing room didn’t work and was handled manually. There were no routines for washing and disinfection between farrowing batches.
Given the per-acute progression of disease, the high mortality and no expected diagnostic laboratory answers due to Easter holiday, a metaphylactic treatment was initiated on day 3. This was also deemed relevant to provide diagnostic information. Half of the piglets (group 1) received intramuscular injections (IM) of 600 mg benzylpenicillin procaine q 24 h for three days. Following penicillin treatment, no piglets died after 12 hours, whereas 50 piglets died during the following night in the untreated group (group 2). Group 2 were then given the same antibiotic treatment on day 4.
After a second rise in piglet mortality on day 9, all piglets were IM injected with 600 mg benzylpenicillin procaine q 24 h for five days. The piglet mortality stopped within twelve hours after the first injections with benzylpenicillin procaine every time a new treatment was initiated (Figure 2).
A daily routine supplying the piglets with iron-supplemented peat on the floor for oral consumption from day 6 and onwards until weaning was established (Figure 2).
The sows with signs of polyarthritis and meningitis were treated with an IM injection of 10,5 g benzylpenicillin procaine q 24 h in three days and a single IM injection of 800 mg ketoprofen. The treated sows had no clinical signs of disease the day after initiated treatment and had no relapse of disease.
Approximately half of the piglets getting their first injection of benzylpenicillin procaine on day 3 and 4 started vomiting within an hour after injection. A few showed central nervous signs, lying in lateral recumbency, with paddling movements of the hind limbs. After a few hours, all of them appeared healthy. None of these died and the next day it was not possible to see which ones had been sick. This was not seen again in the subsequent treatment.