Infectious diseases of swine 2/2 Flashcards
Describe the etiology of seneca valley virus.
Senecavirus A from genus Senecavirus, family Picornaviridae.
Most cases seem to occur between spring and fall.
The virus has potent oncolytic abilities, explored in human cancer treatment research.
Morbidity & Mortality of seneca valley virus.
Morbidity in neonates can reach 70%
Mortality ranges from 5–60%
Associated with pig neonatal mortality (epidemic transient neonatal losses, ETNLs).
Describe transmission of seneca valley virus.
Transmission is not well understood. NOT zoonotic though.
Direct and indirect transmission likely play a role.
Vertical transmission may occur.
Clinical signs of seneca valley virus infection. (5+)
Pyrexia
Anorexia
Lameness
Vesicles (blisters) or ulcers on snout, mouth, tongue, and hooves at the coronary band or in between the hooves.
Cutaneous, enteric, and neurological disorders.
Clinical signs may persist for 2–14 days.
Post-mortem lesions of seneca valley virus infection. (3+)
Petechial hemorrhages of the kidneys
Interstitial pneumoonia
Ulcerative lesions in urinary bladder, choroid plexus, renal pelvis, oral mucosa.
What should you use to diagnose seneca valley virus?
Lungs, lymph nodes, liver, spleen, small and large intestines, and tonsils between 3 and 5 days post infection.
Oral and nasal secretions and also in feces up to 28 days post inifection.
- Electron microscopy, immunohistochemistry
- RT-PCR
- ELISAs
- Virus neutralization
How can you prevent seneca valley virus?
No vaccines available.
No tx available.
You’re out of luck!
Teschen disease also goes by the following names: (5)
Talfan disease
Benign enzootic paresis
Poliomyelitis suum
Teschovirus encephalomyelitis
Teschen / Talfan
Describe the etiology of Teschen disease.
Cause by porcine Teschovirus, 11 serotypes.
There are highly virulent and mildly virulent variants.
Small dose of infected feces is enough for spread of infection.
Probably exists worldwide.
Course of disease in Teschen disease.
Most infections are subclinical.
Clinical disease outbreaks are rare.
The name Teschen disease is traditionally used for the most severe form of the disease.
Pathogenesis of Teschen disease.
Multiplies in large intestine and ileum, mucosal lymphoid tissues and lymph nodes for several weeks.
Shed in large quantities in the faeces.
In weaners the virus is able to multiply in the intestines but it cannot get to the nervous system (due to sow’s colostral antibodies which are still circulating in the pig’s blood stream).
If it manages to reach the CNS (due to a lack of aB), it multiplies in the nerves and causes damage.
- If mother has never been infected with the virus
- If the newborn piglet didn’t get enough colostrum
- If the virus enters a naive herd for the first time
Clinical signs of Teschen disease.
Directly analogous to human poliomyelitis.
Slight anorexia and pyrexia for a day. Drunken swaying gait.
Ascending paralysis of muscles which may progress to a complete hind end paralysis. Eventually, can’t rise from a dog-sitting position. Incoordination.
Infection of the motor nerves only and not the sensory nerves. The pig still have sensation and can feel pin pricks.
In the severe form of the disease, the motor nerves are completely destroyed; fever, ataxia, seizures, convulsions, opisthotonos, coma and death; mortality is high.
Which pigs recover spontaneously from Teschen’s disease?
In weaners it does not often progress to full paralysis, just a drunken swaying gait. They can recover.
Post-mortem lesions of Teschen disease?
Typical lesions of any virus but are not specific to the Teschen disease.
No microscopic lesions in other organs.
Spinal cord, ventral horns: Neuronal necrosis, multifocal, marked, with gliosis, satellitosis, neuronophagia, and dorsal funiculi axonal degeneration.
How do you diagnose Teschen disease?
Clinical signs are suggestive but not conclusive.
Antibody titer in paired blood samples helps.
At the start of the disease and 10-14 days later.
Microscopic examination of the brains and spinal cord lend evidence.
How do you prevent Teschen disease? (3)
Vaccine none available commercially.
Colostral immunity would help prevent it but requires either vaccine which isn’t available, or sow infection.
Hygiene
Etiology of african swine fever.
African swine fever virus from genus Asfivirus, family Asfarviridae.
Ticks of the genus Ornithodoros are considered the natural arthropod host.
Transmission: arthropod vectors + direct & indirect contact.
IP of african swine fever.
IP usually 4–19 days; acute form 3–4 days.
Peracute form (highly virulent virus) just sees sudden death with few signs.
Clinical signs of acute african swine fever virus. (6+)
Fever (40.5–42°C)
Early leukopenia and thrombocytopenia (48–72 hours).
Increased pulse and respiratory rate.
Reddening of the skin (white pigs) – tips of ears, tail, distal extremities, ventral aspects of chest and abdomen.
Vomiting, diarrhoea (sometimes bloody) and eye discharges may occur. Abortion may occur in pregnant sows.
Anorexia, listlessness, cyanosis and incoordination within 24–48 hours before death.
Death within 6–13 days, or up to 20 days.
In domestic swine, the mortality rate often approaches 100%!
Clinical signs of subacute african swine fever virus.
Less intense signs; slight fever, reduced appetite and depression.
Duration of illness is 5–30 days.
Abortion in pregnant sows.
Death within 15–45 days.
Mortality rate is lower (e.g. 30–70%, varies widely).
Clinical signs of chronic african swine fever virus.
Loss of weight
Irregular peaks of temperature
Respiratory signs
Necrosis in areas of skin
Chronic skin ulcers
Arthritis
Pericarditis
Adhesions of lungs
Develops over 2–15 months
Low mortality
Post-mortem lesions on african swine fever.
Pronounced haemorrhages in the gastrohepatic and renal lymph nodes.
Petechial haemorrhages of the renal cortex, also in medulla and pelvis of kidneys.
Congestive splenomegaly
Oedematous areas of cyanosis in hairless parts.
Cutaneous ecchymoses on the legs and abdomen.
Acute form:
* Excess of pleural, pericardial and/or peritoneal fluid.
* Petechiae in the mucous membranes of the larynx and bladder, and on visceral surfaces of organs.
* Oedema in the mesenteric structures of the colon, gallbladder and adjacent to the gall bladder.
Chronic form:
* Focal caseous necrosis and mineralisation of the lungs may exist.
* Lymph nodes enlarged
Ddx for african swine fever. (7)
Classical swine fever (CSF or hog cholera)
Porcine reproductive and respiratory syndrome (PRRS)
Erysipelas
Salmonellosis
Aujeszky‟s disease (or pseudorabies) [younger swine]
Pasteurellosis
Other septicaemic conditions
How do you diagnose african swine fever?
Blood collected during the early febrile stage in EDTA tube.
Spleen, lymph nodes, tonsil and kidney kept at 4°C.
Or serum collected within 8–21 days after infection in convalescent animals.
Isolate the virus or detect antigens/viral DNA.
Or, detect antibodies.
