Swine Pleuropneumonia – Infections Example

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"Swine Pleuropneumonia" is a marvellous example of a paper on infections. Swine pleuropneumonia or procine pleuropneumonia is caused by the bacteria Actinobacillus pleuropneumoniae. Actinobacillus pleuropneumoniae is a Gram-negative, facultative bacteria. The disease is a highly contagious disease among swine and has several clinical implications as well. The bacterium was first associated with the disease in the year 1964 when porcine in Argentina were severely afflicted by a fatal, epidemic respiratory disease (Shope, 1964). The bacterium was previously known as Haemophilus pleuropneumoniae but was later re-classified after DNA studies were conducted showing its genotypic proximity to the genus- Actinobacillus.

A. pleuropneumoniae belongs to the order Pasteurellales and Family Pasteurellaceae. Pathobiology   and Pathogenesis The bacterium causes fibrino-hemorrhagic necrotizing pleuropneumonia among porcine herds. Research studies have indicated the role played by various molecular factors underlying the infection. One of the prime components of pathogenesis is lipopolysaccharide endotoxin which is a heat-labile factor mostly involved in initiating the development of lesions in the lungs during the acute phase of infection(Udeza et al, 18987). Another equally important role in the pathogenesis is played by the A. pleuropneumoniae exotoxin ApxI.

Studies conducted using RT-PCR and ELISA analysis shows that the exotoxin stimulated the macrophage of the infected porcine to transcribe mRNAs of IL-1β , IL-8 and TNF-alpha thereby inducing the expression of these genes (Chen et al, 2011). Furthermore, the exotoxin delineated various signalling pathways underlying the expression of cytokines. Epidemiology Swine plueropneumonia is widely found disease among pig herds in all parts of the world. It is an airborne infection which is transmitted through the nose to nose contact. In the U. S. alone 80% of the farms are infected even though only 20% show clinical manifestations of the disease. Symptoms The onset of the disease is sudden in most cases and among some groups pig may die without showing any clinical symptoms at all.

The course of the disease may be peracute, acute or chronic and the manifested clinical signs and symptoms depend on the course of the disease. In its acute form pigs mostly between the age span of 8-16 weeks and still weaning when affected by the bacterium do not show profound clinical manifestations. Sudden death is the most common clinical symptom of the acute form which is also accompanied by frothing and oozing of blood from the nose.

When alive the pigs may be depressed, lack appetite, run a high fever and suffer from cough-like symptoms. However, the most important clinical manifestation of the infection is respiratory distress in live swine. Pigs gradually have difficulty in breathing and are involved in open-mouth breathing. In the chronic form alongside these symptoms, lesions are also observed bilaterally. The lesion is usually fibrin necrotic and haemorrhagic in nature. This may also be accompanied by pleuritis and pericarditis.

In the severe forms both in acute and chronic cases the lungs become swollen and start to ooze blood. The only observable difference between the chronic and acute form is in the organization of the lesions. In the chronic form, the lesions are more localized and are more organized when compared to the acute form of infection in the swine herds.   Serotypes and Serology There exists a number of different serotypes and not all of the strains are involved in causing the disease among pigs. Studies have shown that there exist 12 different serotypes and 2 sub-types of Actinobacillus pleuropneumoniae (Frey and Nicolet, 1990).

Serotypes 1, 5 and 7 are found most prevalently in the United States. The serotype present in a particular pig is one of the major factors contributing to the manifestation of the clinical symptoms. Serotype 1 is known to be highly virulent, while 2,5,9, 10 and 11 are moderately virulent and serotypes 3, 6, 7, and 12 are the least virulent forms. However, regardless of the type of serotype present in the pig’ s bloodstream the severity of the disease developed depends on the exposure to the pathogen, dosage and susceptibility of an individual pig to the pathogenic bacteria (Marstellar and Fenwick, 1999). Diagnosis and Treatment Diagnosis is basically conducted upon observing the clinical symptoms and appearance of gross lesions in the pigs.

However concurrent infections by other pathogens may also complicate the diagnosis in some rare cases. Therefore, molecular approaches and basic serological tests are employed for accurate and proper diagnosis of the disease. Submission of sample to clinical laboratories to determine the antibiotic sensitivity of the pathogens may be used for proper identification.   One of the most useful and accurate diagnostic assays is Enzyme-Linked Immuno-sorbent Assay or ELISA while in some cases PCR testing is also employed.

In some rare cases antigenic crossreactivity between the toxins produced may complicate accurate detection and diagnosis and therefore in such rare cases special ELISA assay such as Capsular Polysaccharide-Biotin-Streptavidin Enzyme-Linked Immunosorbent Assay is employed (Inzana and Fenwick, 2001). The most widely used treatment form employed today is the usage of antibiotics such as tetracycline, tylosin, sulphonamides, synthetic penicillin etc. , during the early stages.

The injection is the best treatment methodology for sick pigs. Prevention There are several ways in which initial preventive measures may be adopted in order to prevent pigs from acquiring infections. One of the most important preventive measures is the usage of vaccines available. T he vaccines may contain both live and attenuated forms of the pathogen. PLEURAvac is an example of a vaccine currently used in countries such as Australia and New Zealand. Research studies have shown that vaccination with proteinase K-treated outer membrane of Actinobacillus (Haemophilus) pleuropneumoniae extended good protection against the disease (Chiang et al, 1991). Studies have established that some medication such as sulfadimethoxine and sulphamethoxazole in combination with trimethoprim may be mixed in the feed of pigs.

This will help in preventing the disease (Mengelers et al, 2000) Other common preventive measures may also be adopted in order to prevent the onset of the disease or the spread of the disease. Overstocking of pigs is to be avoided and pig broods should not be mixed after weaning. The pens where the pigs are kept need to be well ventilated and cleaned on a regular basis.

The pigs should be given clean food and water and their health need to be monitored regularly.


Chen,Z-W., et al. (2011). Mechanisms underlying Actinobacillus pleuropneumoniae exotoxin ApxI induced expression of IL-1β, IL-8 and TNF-α in porcine alveolar macrophages. Vetrinary Research, 42 (25). http://www.veterinaryresearch.org/content/42/1/25

Chiang, Y.W., et al.(1991). Improved protection of swine from pleuropneumonia by vaccination with proteinase K-treated outer membrane of Actinobacillus (Haemophilus) pleuropneumoniae. Vet Microbiology, 27 (1), 49-62.

Frey,J. And Nicolet,J.(1990). Hemolysin patterns of Actinobacillus pleuropneumoniae.Journal of Clinical Microbiology, 28 (2), 232-236.

Inzana,T.J. and Fenwick,B.(2001). Serologic Detection of Actinobacillus pleuropneumoniae in Swine by Capsular Polysaccharide-Biotin-Streptavidin Enzyme-Linked Immunosorbent Assay. Journal of Clinical Microbiology, 39 (4), 1279-1282. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC87924/

Marstellar,T.A. and Fenwick,B. (1999). Actinobacillus pleuropneumoniae disease and serology.Swine Health Prod., 7(4),161–165. https://www.aasv.org/shap/issues/v7n4/v7n4p161.pdf

Mengelers, M.J., et al. (2000). Prevention of pleuropneumonia in pigs by in-feed medication with sulphadimethoxine and sulphamethoxazole in combination with trimethoprim.The Vetrinary Quaterly, 22 (3), 157-162.

Shope,R. (1964).Porcine Contagious Pleuropneumonia I. Experimental, Transmission, Etiology, and Pathology. JEM Home, 119 (3), 357-368.

Udeza,F.A., Latimer,K.S. and Kadia,S. (1987). Role of haemophilus pleuropneumoniae lipopolysaccharide endotoxin in the pathogenesis of porcine Haemophilus pleuropneumonia.American Journal of Veterinary research, 48 (5), 768-773.

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