The clinical disease in pigs
Other susceptible domestic species
Necropsy findings in pigs
The epidemiological pattern of the disease
There are no pathognomonic features ascribable to Nipah virus disease in pigs. Differential diagnoses should include the following:
- Classical swine feverWhile not pathognomonic, disease in sows may support a presumptive diagnosis of Nipah virus. Severe respiratory symptoms, neurological symptoms, or increased mortalities in sows are not common features of other diseases.
- Porcine reproductive and respiratory syndrome
- Aujeszkys disease (Pseudorabies)
- Swine enzootic pneumonia due to Mycoplasma hyopneumoniae
- Porcine pleuropneumonia due to Actinobacillus pleuropneumonia
Nipah virus will infect pigs of all ages. Clinical observations in the Malaysian outbreak suggested a different clinical picture in different classes of animals. For example, sows were noted to present primarily a neurologic syndrome and porkers a respiratory syndrome. It may also be that observed clinical signs reflected another variable such as husbandry. For example, the housing of sows and boars in stalls which precluded substantial exercise may have masked respiratory involvement.
Clinical observations in weaners and porkers:
Affected weaners and porkers showed acute febrile illness with respiratory signs ranging from rapid and laboured breathing to harsh non-productive coughing. In severe cases, there was blood-tinged mucous discharge from the nostrils. In less severe cases, open mouth breathing was a feature. Neurological signs were also observed, and included trembling, twitching, muscular spasms, rear leg weakness and varying degree of lameness or spastic paresis.
Clinical observations in sows and boars:
Affected sows and boars were found dead overnight, or exhibiting acute febrile illness with laboured breathing (panting), increased salivation and serous, mucopurulent or blood-tinged nasal discharge. Neurological signs including agitation and head pressing, tetanus-like spasms and seizures (Figure 3), nystagmus, champing of mouth, and apparent pharyngeal muscle paralysis were observed. Abortions were reported in affected sows.
Figure 3: Acute onset neurological signs including seizures, tetanic-like spasms and jaw champing are seen in sows
Clinical observations in suckling pigs:
Mortality of suckling pigs was estimated to be 40 percent. The relative contribution of the effects of infection in suckling pigs and sow inability to nurse is unknown. Healthy but confirmed seropositive sows were observed to nurse healthy piglets. Most of the infected piglets showed symptoms of open mouth breathing, leg weakness with muscle tremors and neurologic twitches.
Clinical disease in pigs can be very subtle and a large proportion of pigs in a farm may not exhibit any clinical signs. The incubation period is estimated to be 7 to 14 days. Transmission studies in pigs in Australia at the CSIRO Australian Animal Health Laboratory established that pigs could be infected orally and by parenteral inoculation. It was observed that infection could spread quickly to the in-contact pigs. Neutralizing antibodies were detectable 10-14 days post-infection.
Some farmers reported deaths in dogs at the same time as in pigs during the Malaysian outbreak. Two such animals exhibiting a distemper-like syndrome were examined. Nipah virus was isolated from the tissues of one and Nipah virus antigen demonstrated in both by immunoperoxidase staining of tissue sections (Chua et al. 2000). Serological surveys of dogs in infected areas showed that up to 50 percent of clinically normal dogs had anti-Nipah virus antibodies by ELISA. Some farmers reported cats to be clinically affected also. The susceptibility of cats was confirmed by experimental infections (Middleton et al. 2001).
Over 3 000 horses in Malaysia were subjected to serological examination (by serum neutralization test). Two of these horses were found to have neutralizing antibodies to Nipah virus. Immunohistochemistry on formalin-fixed tissues from a third horse with a history of neurological symptoms showed Nipah virus infection. All three horses were from a single property surrounded by infected pig farms.
A survey of ubiquitous peridomestic small mammals including rodent and bird species on and around infected pig farms found no evidence of infection.
Necropsies should be conducted of recently dead and acutely diseased pigs. Animals chosen should be representative of the affected ages and types, and should include a number of animals to increase the sensitivity of the sampling procedure.
The post-mortem findings due to Nipah virus infection in pigs are relatively non-specific. The lung and the meninges were the key organs affected. The majority of the cases showed mild to severe lung lesions with varying degrees of consolidation, emphysema and petechial-to-ecchymotic haemorrhages, and blood-tinged exudates in the airways. On cut surface, the interlobular septa were distended. The meninges showed generalized congestion and oedema. Other visceral organs were apparently normal.
Clinical disease consistent with case descriptions across all classes of pigs, and a history of introduction of new pigs constitutes a suspicious epidemiological pattern. An increased incidence of sow illness and death should be treated with particular suspicion. Simultaneous reports of unexplained illness or deaths in dogs or cats should strengthen consideration of Nipah virus infection, as should concurrent human disease characterized by early signs of encephalitis (Chua et al. 1999) on a suspected farm. In human cases, the observed incubation period ranges from 4 to 18 days with the first symptom being a severe headache. Farm workers have been reported to develop illness after pigs have recovered.
Nipah virus in Malaysia was spread from farm to farm by the movement of infected pigs. The extensive testing and surveillance programme which followed the outbreak control programme showed that farms that did not receive pigs generally remained uninfected, even when an adjacent farm was infected. Thus, a check for any violation of farm biosecurity should be conducted where Nipah virus is suspected. Also, farms which took prompt action to cull populations of grower pigs from suspected sources also avoided infection with Nipah virus, where growers and breeders were housed separately.
As Nipah virus infection has now been eradicated from the Malaysian pig herd, it is most probable that any new outbreaks will reflect another spillover of the virus from the wildlife reservoir. Thus any future investigation might consider whether contact between the affected pigs and fruit bats may have occurred, although this scenario would only be relevant for the first premises to be infected. Factors to consider would be the system of housing of the pigs, and the presence of fruit or flowering trees that could attract foraging bats to the vicinity of the farm.