Medicina pediátrica en pequeños animales
Presentation
Enfermedades infecciosas del ganado porcino
Cinta Prieto Suárez Francisco Javier Martínez Lobo Joaquim Segalés i Coma
brochure
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Infectious
diseases
of swine
Cinta Prieto Suárez Francisco Javier Martínez Lobo Joaquim Segalés i Coma
19/08/16 13:30
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El objetivo de los autores es editar un manual que resuma de forma clara y concisa las enfermedades mediante la inclusión de numerosas infografías, diagramas de flujo e imágenes que permitan conocer de forma rápida las características más relevantes de las enfermedades porcinas y su control.
Infectious
Cinta Prieto Suárez Francisco Javier Martínez Lobo Joaquim Segalés i Coma
La presente obra constituye un manual de consulta práctico, en el que se describen los aspectos básicos de las enfermedades infecciosas porcinas (etiología, epidemiología, patogenia, cuadro clínico, diagnóstico, tratamiento y prevención) tratados de forma esquemática y visual para abordar, en último lugar, el control de la enfermedad en función de las características del agente causal y de las particularidades de la respuesta del individuo a la infección. Las enfermedades se han elegido por su repercusión sanitaria o económica, y se han agrupado según el grupo de población afectado y el cuadro clínico, con el fin de facilitar el diagnóstico diferencial.
diseases
of swine
Enfermedades infecciosas del ganado porcino
Infectious diseases of swine
Cinta Prieto Suárez Francisco Javier Martínez Lobo Joaquim Segalés i Coma
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AUTHORS: Cinta Prieto Suárez, Francisco Javier
Martínez Lobo and Joaquim Segalés i Coma
FORMAT: 22 x 28 cm. NUMBER OF PAGES: 192. BINDING: hardcover.
ESTIMATED RETAIL
RETAIL PRICE PRICE
75 75€ €
This book is a practical reference handbook, in which the basic aspects of swine infectious diseases are described (aetiology, epidemiology, pathogenesis, clinical picture, diagnosis, treatment and prevention) and explained schematically and visually, to finally deal with the control of the diseases according to their causal agent’s characteristics and the peculiarities of the individual’s response to the infection. The diseases have been chosen because of their sanitary and economic repercussion and have been classified according to the affected group of population and clinical picture, so as to facilitate their differential diagnosis. The aim of the authors was to publish a handbook that would summarise swine infectious diseases in a clear and concise manner by means of numerous infographics, flow diagrams and images, to allow readers to know rapidly the most relevant characteristics of these diseases and their control.
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Presentation of the book Swine veterinary practice has undergone great changes in the last few years. This is essentially due to the appearance of new diseases, which have become a source of concern for swine veterinary practitioners, as they affect pig production noticeably. Furthermore, within this context, a series of advances were made in the control and eradication of other diseases that had been the centre of attention for decades. In this sense, the development of more accurate tools to measure the immune response of animals, a better knowledge of the different agents’ pathogenic mechanisms and the development of new vaccines and immunisation protocols have contributed to the implementation of control strategies for the main diseases affecting pigs. The main objective of this book is to summarise, in a clear and concise manner, the current knowledge available on the main infectious diseases that affect pigs for a rational, accurate and efficient approach of their control, based on the knowledge of both the pathogenic agent’s action on the host and this latter’s response to the infection. Regarding its structure, the book includes a description of the main infectious diseases that affect pigs, classified according to the age group they affect and the type of clinical signs they cause, with the final objective of facilitating their differential diagnosis. The choice of diseases to study is based on their sanitary and/or economic relevance and, in the case of exotic diseases, on the potential risk they represent for the herd. This work does not aim to be an extensive treatise in which each of the diseases is described in great details, as we believe this need has already been covered by numerous specialised publications that explain the different aspects considered in this book in a monographic and meticulous manner. On the contrary, this work aims to be a practical reference handbook based on the authors’ academic and professional experience, in which the different diseases are described schematically and visually, although with all the basic aspects we believe a professional should know. This structure aims at making the information easy to access to those swine veterinary practitioners who are looking for a quick way to know the most relevant characteristics of the main diseases of swine and their control. This handbook may also be of great help to veterinary students, as they will find, in a summarised and practical manner, all the information necessary to understand the pathogenic action of infectious agents, how pigs respond to these aggressions and how to approach the diagnosis and control of the diseases they cause. Cinta Prieto Suárez
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Infectious diseases of swine
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The authors Cinta Prieto Suárez She graduated in veterinary medicine from the Complutense University of Madrid (UCM) in 1992 and obtained her PhD from the same university in 1997. After obtaining her PhD, she went on to work as a veterinary surgeon and production supervisor in several companies dedicated to swine production and as a member of the swine technical services of an important veterinary pharmaceutical company. In 2002, she came back to the UCM, where she is currently working as a professor at the Department of Animal Health. Her teaching focuses on the fields of infectious diseases, preventive medicine and swine production medicine. She also teaches several aspects of swine production and health in a Master’s Degree programme. Her research work has focused, since her doctoral studies, on the study of several topics related to the porcine reproductive and respiratory syndrome virus, from the pathogenesis of the infection to the variability of the virus and its repercussions on virulence, immunogenicity and crossed protection. Cinta Prieto has been a diplomate of the European College of Porcine Health Management since 2008.
Francisco Javier Martínez Lobo He graduated in veterinary medicine from the Complutense University of Madrid (UCM) in 2004 and obtained his PhD in veterinary medicine from the same university in 2010. He has done internships in companies dedicated to swine production and pharmaceutical companies, and was a visiting student at the University of Nebraska (USA). He is currently working at the Department of Animal Health of the University of León Faculty of Veterinary Medicine. He has collaborated as an undergraduate professor of Infectious Diseases, Preventive Medicine and Swine Production Medicine both at the Complutense University of Madrid and at the University of León and has taught the subject Alterations of Reproduction in Livestock in a postgraduate programme (Master’s Degree level).
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Infectious diseases of swine
His research work focuses on the study of the porcine reproductive and respiratory syndrome virus at the Complutense University of Madrid, and on the study of swine enteric diseases and more specifically on swine dysentery at the University of León. He has been a diplomate of the European College of Porcine Health Management since 2013.
Joaquim Segalés i Coma Joaquim Segalés graduated in veterinary medicine from the Autonomous University of Barcelona (UAB) in 1991. In 1996, he was awarded a PhD from the same university, after conducting his PhD research at the University of Minnesota for 15 months. Since 1996 he has been working as a professor of swine pathology and clinical medicine at the UAB. From 1996 to 2012 he was responsible for swine disease diagnosis at the Department of Animal Health and Anatomy of the UAB. In 2000 he joined the Centre de Recerca en Sanitat Animal (CReSA, Animal Health Research Centre) as a researcher and has been the director of the centre since 2012. He was board certified by the European College of Veterinary Pathologists (ECVP) in 2000 and is a founder member of the European College of Porcine Health and Management.
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Presentation brochure PDF format. El objetivo de losinautores es editar un manual que resuma de
I
formaCV. clara y concisa las enfermedades mediante la inclusión de Author´s
numerosas infografías, diagramas de flujo e imágenes que permitan conocer de forma rápida las características más relevantes de las enfermedades porcinas y su control.
Sample chapter compatible with iPad.
www.grupoasis.com/promo/infectious_diseases_swine
Cinta Prieto Suárez Francisco Javier Martínez Lobo Joaquim Segalés i Coma
Communication services
Enfermedades infecciosas del ganado porcino
La presente obra constituye un manual de consulta práctico, en el que se describen los aspectos básicos de las enfermedades infecciosas porcinas (etiología, epidemiología, patogenia, cuadro clínico, diagnóstico, tratamiento y prevención) tratados de forma esquemática y visual para abordar, en último lugar, el control de la enfermedad en función de las características del agente causal y de las particularidades de la respuesta del individuo a la infección. enfermedades se han elegido por su repercusión sanitaria o WebLas site económica, y se han agrupado según el grupo de población afectado Online of the chapter. y elvisualisation cuadro clínico, consample el fin de facilitar el diagnóstico diferencial.
tious_diseases_swine_cover.indd 1
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Francisco Javier Martínez Lobo Joaquim Segalés i Coma
Infectious
diseases
Enfermedades infecciosas del ganado porcino
of swine
Cinta Prieto Suárez Francisco Javier Martínez Lobo Joaquim Segalés i Coma
19/08/16 13:25
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Table of contents 1. Vulvar discharge syndrome 2. Postpartum dysgalactia syndrome 3. Swine brucellosis 4. Porcine parvovirus infection and enterovirus infection (SMEDI syndrome) 5. Porcine reproductive and respiratory syndrome 6. Aujeszky’s disease 7. Swine streptococci 8. Glässer disease 9. Exudative epidermitis 10. Diarrhoeas caused by rotaviruses 11. Clostridial diseases 12. Neonatal diarrhoeas caused by E. coli 13. Post-weaning colibacillosis and oedema disease 14. Transmissible gastroenteritis 15. Epidemic diarrhoea
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16. Swine dysentery 17. Porcine proliferative enteropathy 18. Salmonellosis 19. Porcine intestinal spirochetosis 20. Swine enteric diseases 21. Swine influenza 22. Atrophic rhinitis 23. Porcine pleuropneumonia 24. Enzootic pneumonia 25. Porcine respiratory disease complex 26. Porcine circovirus 27. Erysipelas 28. Classic swine fever 29. African swine fever 30. Swine vesicular diseases: swine vesicular diseases, vesicular stomatitis, foot-and-mouth diseases, vesicular exanthema of swine, swinepox
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Infectious diseases of swine
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GLĂ„SSER DISEASE Infectious bacterial disease characterised by the appearance of fibrinous polyserositis and polyarthritis in affected pigs.
AETIOLOGY
FIGURE 1. Haemophilus
parasuis.
Despite the importance of correctly classifying isolates, there is no clear correlation between serotype, genotype, and virulence of H. parasuis isolates.
This disease is caused by Haemophilus parasuis, a small, Gram-negative bacillus of the family Pasteurellaceae that shows high genomic heterogeneity. It is a difficult microorganism to isolate as it requires nicotinamide adenine dinucleotide (NAD) or Factor V for growth. Isolation thus requires the use of supplemented media or chocolate agar, in which small, greyish-brown colonies form. H. parasuis shows significant genomic, serological, and pathogenic diversity. Fifteen serotypes and a large number of nontypeable isolates have been documented. From a pathogenetic perspective, isolates identified can be classified as avirulent (i.e. colonise the respiratory tract) or virulent (i.e. capable of systemic diffusion). Classification of the bacteria is very important for diagnosis, given the existence of avirulent strains, and for disease control, as cross-protection between isolates is limited.
EPIDEMIOLOGY H. parasuis is part of the respiratory microbiota of the pig, its natural host. The most prevalent serotypes are 4 and 5, followed by nontypeable serotypes. Colonisation occurs very early; H. parasuis is the most prevalent agent in 1-week-old suckling pigs, although maternal immunity prevents the development of disease at early ages (Fig. 2).
Colonisation in the presence of maternal immunity decreases the incidence of the disease after maternal immunity has disappeared. It is possible to isolate distinct strains from healthy animals on the same farm. Moreover, the isolation of more than one strain in a single individual and the substitution of certain
FIGURE 2. Maternal immunity prevents the occurrence of disease in young animals.
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Glässer disease
strains by others over time are commonly observed. However, in cases of disease a single strain is usually involved. The process usually develops during the transition phase, when maternal immunity decreases and virulent strains spread to pigs that lack immunity. Predisposing factors, which decrease the immune response to suckling pigs, as well as other pathogens are implicated in disease onset (Fig. 3).
flammatory reaction that manifests as fibrin deposition and fluid accumulation (Fig. 4d).
CLINICAL PRESENTATION AND LESIONS H. parasuis infection has various clinical forms.
PATHOGENESIS
HYPERACUTE FORM
1. The natural route of infection is oronasal. H. parasuis colonises the nasal and tracheal epithelium. Colonisation of the upper respiratory tract can result in rhinitis and impaired mucociliary function, and leads to a carrier state (Fig. 4b). 2a. H. parasuis reaches the lung, where avirulent strains are phagocytosed and eliminated by alveolar macrophages (Fig. 4b). 2b. Virulent strains resist phagocytosis, probably due to their expression of the capsule, invade endothelial cells, and spread throughout the body via the lymphatic or haematic routes, a process facilitated by the virus’ resistance to the action of complement (Fig. 4c). 3. The septicaemic process culminates with the arrival of H. parasuis to internal organs, where it exerts its pathogenic effect, replicating in serous surfaces such as the meninges, endocardium, peritoneum, etc., and inducing an in-
Environmental factors: ■■ Low
Infected animals show high fever and anorexia, but often cyanosis and sudden death are the only signs observed. The lesions are relatively inapparent and, if present, are compatible with septicaemic processes, e.g. disseminated intravascular coagulation, endotoxic shock, petechiae, ecchymoses and/or fibrinous thrombi in various organs, serofibrinous or fibrinopurulent exudate in the cavities, and meningitis.
Not all clinical signs are observed in the same animal.
GLÄSSER DISEASE Animals can show high fever, anorexia, joint swelling, abdominal breathing, and nervous signs such as tremors and incoordination, but not all signs are necessarily observed in the same animal. These clinical findings are associated with serous inflammation, such as meningitis, fibrinous pleuritis,
Strain virulence
Circulation of virus: ■■ PRRS ■■ Circovirus
temperatures
■■ Humidity ■■ Insufficient ventilation
Glässer disease
Immune status: ■■ Poor
maternal immunity
■■ Poor
Social stress: ■■ High
population density
■■ Mixing
of animals of different origins
cross-protection
FIGURE 3. Predisposing factors involved in the onset of disease.
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fibrinous pericarditis, polyserositis with the presence of serofibrinous or fibrinopurulent exudate in the cavities, and polyarthritis. Affected animals may overcome the acute phase of the disease and enter a chronic phase, primarily characterised by stunting and arthritis.
a
PNEUMONIA H. parasuis can induce a catarrhal/purulent or, less commonly, fibrinous/haemorraghic bronchopneumonia, characterised by cranioventral consolidation of the pulmonary lobes. Coughing, shortness of breath, and weight loss are observed in affected animals. Furthermore, H. parasuis is often found as a secondary agent in porcine respiratory disease complex.
b
1
2 1 Avirulent strains 2 Virulent strains
c
FIGURE 5. Sudden death with signs of septicaemia in a hyperacute
case.
d
Inflammatory reaction
FIGURE 4. Disease development.
FIGURE 6. Accumulation of fluid in the peritoneal cavity of the animal from the previous image.
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Glässer disease
FIGURE 7. Nervous symptoms in an affected suckling pig.
FIGURE 8. Ascites fluid in a dead pig.
FIGURE 9. Fibrinous pericarditis.
FIGURE 10. Fibrin residues in the liver.
FIGURE 11. Purulent meningitis in a suckling pig with nervous signs. Image courtesy of Micros Veterinaria, León.
FIGURE 12. Fibrinous pneumonia in the cranial lobes of the lung of an animal with respiratory signs. 5
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DIAGNOSIS Diagnosis is based on the clincal signs and lesions observed, as well as the age of onset. However, several pathological processes have similar presentations, especially oedema disease, swine streptococcal infections, and infections caused by certain mycoplasma such as M. hyorrhinis and M. hyosynoviae.
AETIOLOGICAL DIAGNOSIS Definitive diagnosis should be aetiological, and is established by isolation or PCR identification of bacteria from cavity exudates or swabs of serosal surfaces obtained from unmedicated animals in the acute phase of the disease. After isolation of the bacteria an antibiogram can be performed to determine the most appropriate treatment and the bacterial serotype, which is useful for epidemiological monitoring and disease prevention by vaccination. Genotyping of the isolated bacteria can also be useful.
Cavity fluids*: ■■ Ascites
■■ Synovial
H. parasuis may be present in the upper respiratory tract of healthy animals and can colonise the lung post-mortem. As a result, swab samples acquired from the nose, tonsils, or lung can lead to misdiagnosis.
Swabs of serous surfaces containing fibrin
fluid
■■ Pericardial
FIGURE 13. Microbiological isolation of H. parasuis by culture in chocolate agar.
Lung
fluid
fluid
Refrigerated transport within 24 hours
False positives: Isolates from the upper respiratory tract
Evaluate the role of H. suis in porcine respiratory disease complex (PRDC)
Antibiogram Characterisation of isolate:
Culture
PCR
■■ Serotyping ■■ Molecular
characterisation
* Cavity fluid samples can be obtained aseptically using a syringe or swab. It is preferable to use swabs with Amies transport medium to ensure preservation of the bacteria until arrival at the laboratory. However, if only PCR analysis is to be performed, swabs can be used without transport medium. FIGURE 14. Sampling in a suspected case of Glässer disease.
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Glässer disease
TREATMENT Individual treatment of affected animals
Collective therapy for entire group
Parenteral administration
Oral antibiotic
Betalactams In cases of meningitis Antibiotics
Anti-inflammatories
Sick animals do not eat or drink. Parenteral treatment is critical for recovery and for hydration.
In water
In feed
Bioavailability, stability, dosage, and treatment time should be taken into account.
FIGURE 15. Possible treatments depending on the number of affected individuals.
PREVENTION AND CONTROL
KEY CONCEPTS FOR THE PREVENTION AND CONTROL OF GLĂ„SSER DISEASE 1. Maintain strict biosecurity measures to prevent the entry of new strains into the farm. 2. Ensure proper intake of colostrum. Maternal immunity protects suckling pigs from developing disease but not from colonisation. Moreover, early colonisation, accompanied by good maternal immunity, decreases disease incidence. 3. Ensure an appropriate breeder balance within the population. A high turnover rate favours litters that are uncolonised and/or lack maternal immunity due to a lack of exposure of sows to the isolates present on the farm. 4. Avoid mixing animals to prevent the spread of pathogenic strains. 5. Control predisposing factors such as temperature, humidity, and ventilation and above all reduce social stress. 6. Strategically administer antibiotics by pulse dosing or continuous administration in feed during the period of risk. Assess the risk of development of antibiotic resistance. 7. Implement vaccination programs when inadequate maternal immunity or exposure to the farm strain are anticipated. The following vaccines can be used: a. Commercial bacterin vaccines, which generally combine two serotypes. These do not protect against all strains, but are useful in some cases. b. Autogenous vaccines prepared with the farm strain. It is important to confirm the identity of the selected pathogenic strain.
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Infectious diseases of swine
21
SWINE FLU Infectious disease of sudden onset and acute course characterised by fever and respiratory signs of varying severity in pigs of all ages.
AETIOLOGY 1
2
3
4 FIGURE 1 1 2
Haemagglutinin Segmented genome
3 4
M protein Neuraminidase
The only subtypes firmly established as pathogens in pigs are H1N1, H3N2, and H1N2.
Swine flu is caused by a pleomorphic, enveloped virus of the family Orthomyxoviridae whose genome consists of eight single-stranded RNA segments of negative polarity. Its 11 proteins include a haemagglutinin (HA) and neuraminidase (NA) (Fig. 1). ■■ Haemagglutinin. Involved in virus entry into the cell. Binds to mannose residues of the sialic acids of the membrane of respiratory epithelial cells. Neutralising antibodies produced against haemagglutinin correlate with protection. ■■ Neuraminidase. Releases the virus from its union to the receptor and is implicated in the release of viral progeny and their dissemination in the respiratory tract. Influenza viruses are classified into three types (A, B, and C), of which only A is relevant in swine. In type A, there are 16 possible haemagglutinins (H) and 9 possible neuraminidases (N), which combine to form distinct subtypes. This combination forms the basis of the official name of the virus, which includes information on the type, species of origin, place of isolation, isolate number, and year of isolation. Thus, the strain A/swine/New Jersey/8/76 is strain 8 of type A isolated from pigs in New Jersey in 1976.
EPIDEMIOLOGY Type A influenza virus can infect many species, although some degree of host restriction has been demonstrated. Mannose can bind to sialic acids via α-2,3 and/or α-2,6 bonds. α-2,3 bonds predominate in birds and horses and α-2,6 bonds in other mammals, although both are well represented in pigs. The predilection of HA for one or other bond type largely determines the specificity of the virus for one host or another.
Anatids appear to be the key factor in the epidemiology of influenza, as they can develop inapparent infections caused by any type A virus. However, because the respiratory epithelium of the pig contains α-2,3 and α-2,6 bonds, it can be infected by viruses of distinct origin, sometimes simultaneously, and hence plays an important role in the generation of new virus variants with the ability to infect not only pigs but also humans (Fig. 2).
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Swine flu
Classic H1N1
H3N2
1983
1968
H1N1
1979 1980s
1994
1990s 2003
H1N2
FIGURE 2. Schematic showing the role played by different species in the epidemiology of swine flu.
One of the most important characteristics of the virus is the continuous emergence of new variants, caused by the combination of two phenomena: a. Antigenic drift: these are changes in amino acids, resulting from the high mutation rate of the virus, that allow it to evade the host’s immune response. b. Genomic reorganisation: these are changes caused by the exchange of fragments of the genome between two viruses infecting the same cell, resulting in the generation of a completely new virus.
H3N2
H1N1
The subtypes circulating in Europe are H1N1, H3N2, and H1N2. The H1N1 subtype that predominates in Europe is derived entirely from an avian virus introduced in 1979. The H3N2 subtype is derived from the 1968 human pandemic “Hong Kong” virus, although numerous genomic reorganisation processes involving human and avian viruses have since occurred. The H1N2 virus has circulated since the mid-1990s. This virus is the result of the recombination of the H3N2 virus with the H1 of a human virus. The latter subunit has since disappeared in swine populations. Other subtypes have been generated as a result of various recombination processes, but have not persisted in pigs in Europe. FIGURE 4. Types of virus currently circulating in European swine.
As an example of genomic reorganisation, Figure 3 shows the source of the H1N1 virus that caused the 2009 pandemic.
Classic H1N1 Triple recombinant American H1N2 H3N2
Eurasian H1N1 of avian origin
+
Pandemic H1N1
=
H1N2 Pigs’ susceptibility to viruses of human and avian origin facilitates simultaneous infection with two different viruses and the generation of new variants.
FIGURE 3. Generation of new viral variants by genomic reorganisation.
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Genomic reorganisation between circulating viruses in Europe (H1N1, H3N2, H1N2) has led to significant antigenic diversity, a key consideration in disease control. Prevalence both on farms and in individuals is very high. Various studies conducted in Spain indicate that over 90 % of farms are infected, with subtype distribution varying depending on the study and the years analysed. However, coinfection with different subtypes is a common finding in all studies.
TRANSMISSION Infected animals excrete the virus in nasal secretions for very short periods (Fig. 5). Transmission can occur: ■■ By direct contact with infected animals during the acute phase. This is a common form of transmission and contributes to the maintenance of the virus on farms. ■■ Through aerosols at close range. This mode of transmission plays an important role in virus persistence on farms and in propagating viral spread between neighbouring farms.
■■
Indirectly, through contact with material contaminated with the virus. Birds excrete the virus in faeces and can contaminate water and the environment. Although rare, contact with contaminated water and direct contact with birds can cause infection of susceptible pigs (Fig. 5).
PATHOGENESIS 1. The virus enters the body via the oronasal route and replicates first in the epithelium of the upper respiratory tract, where it produces lesions in the epithelium and causes loss of cilia (Fig. 6b). 2. After infection of the upper respiratory tract, the virus replicates in the lower respiratory tract, especially in the bronchial, bronchiolar, and alveolar epithelia (Fig. 6b). 3. The infection causes the release of IFN-α and proinflammatory cytokines (TNFα, IL-1, IL-6, and IL-12). These cytokines cause severe inflammation with massive neutrophil infiltration (Fig. 6c) and are responsible for the characteristic systemic signs (fever, lethargy, and anorexia) and respiratory dysfunction.
Direct contact
Contact with contaminated water
Aerosols (short distances)
FIGURE 5. Routes of transmission of swine flu.
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Swine flu
Infection is restricted to epithelial cells of the respiratory system, with no systemic dissemination. The disease course is highly acute, with resolution within a week.
CLINICAL SIGNS AND LESIONS
a
The clinical signs observed strongly depend on the presentation (epidemic or endemic), i.e. the prior immunity of the population.
EPIDEMIC FORM Systemic signs are observed, and may include anorexia, generalised depression, and high fever. In breeding sows intense fever can affect the return to oestrus and cause miscarriages, with foetuses showing no signs of lesions. Boars may show alterations in sperm quality. Respiratory symptoms may include conjunctivitis, rhinitis, and nasal discharge, together with tachypnoea that rapidly evolves to cough and dyspnoea. Morbidity is very high and mortality variable, depending on the development of complications, but is generally low in adults and higher in growing animals. The disease course is very acute, with resolution within 5 to 7 days. The characteristic lesion is a bronchial/interstitial pneumonia with clearly demarcated areas of consolidation that generally affect the apical and middle lobes and, less frequently, the caudal lobes (Figs. 7 and 8). In severe cases, interlobular oedema and the presence of fibrinous exudate in the airway may be observed. These lesions are accompanied by the following microscopic findings: bronchiolitis, necrosis of the alveolar epithelium, and desquamation of the bronchial epithelium, with the presence of cellular debris and inflammatory cells in the airway and alveolar lumen (Fig. 9).
b
c
ENDEMIC FORM
Proinflammatory cytokines
This clinical form is very common on farms due to the high prevalence of the disease. The clinical signs associated with infection are very mild, and often the infection follows a subclinical course. However, in these cases it is necessary to elucidate the role that infection could play in the development of porcine respiratory disease complex (PRDC).
FIGURE 6. Evolution of infection via the airways. 11
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Infectious diseases of swine
FIGURE 7. Multifocal areas of lung consolidation in the cranioventral area that also extend towards the diaphragmatic lobe. The lack of clear delineation of the lesion is highly suggestive of bronchial/interstitial pneumonia.
The clinical course of the epidemic form is very acute, with recovery within 5 to 7 days. The endemic form is characterised by subclinical infection.
FIGURE 9. Lung of swine flu-infected pig with bronchial/interstitial pneumonia. Marked and extensive necrosis of the bronchiolar epithelium and the remains of necrotic material in alveoli near the bronchioles are evident. Haematoxylin-eosin.
FIGURE 8. Lung of suckling pig displaying moderate to marked cranioventral lung consolidation with a multifocal distribution in the apical and middle lobes and in the cranial portion of the left diaphragmatic lobe. Lesions are suggestive of bronchial/interstitial pneumonia due to influenza virus infection.
DIAGNOSIS Definitive diagnosis requires detection of the causative agent as seroprevalence is very high and clinical suspicion is only useful in epidemiological cases. Detection can be performed using samples acquired from live or dead animals. The sample types recommended are nasal or pharyngeal secretions from live animals and lung samples from dead animals. In all cases, it should be borne in mind that the choice of the sample is key, given the short period of virus replication and excretion. Different diagnostic techniques can be used to analyse clinical samples (Fig. 10): ■■ Isolation and viral identification. This requires more time and greater infrastructure, but allows virus typing using molecular or immunological techniques. ■■ RT-PCR. For detection and subsequent typing of type A virus. This is a fast and very sensitive method, but has the disadvantage that it can occasionally detect noninfectious virus. ■■ Immunochromatography for the detection of type A virus. Results are acquired immediately, without the need for laboratory infrastructure. However, sensitivity is relatively low and this approach does not allow viral typing.
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