The Pasteurellaceae and infectious respiratory diseases
Introduction
Members of this family are gram-negative, non-motile, non-spore forming small rods or cocci that tend to stain well at the ends of the bacteria with a clear central zone (bipolar staining). They are facultative anaerobes, nutritionally fastidious, fermentative, and nitrate and oxidase-positive. They are usually inhabitants of the mucosa (oro-pharyngeal, nasal, urogenital) of warm-blooded animals.
The family consists of 38 genera. Agents in this family most frequently cause respiratory tract disease and occasionally reproductive tract disease. Outbreaks of disease occur in stressed, young animals in intensive farming practices.
The Pasteurellaceae are generally very delicate and will only survive for a short period of time in the environment. Thus infections caused by these agents tend to be spread by close contact or by air-borne droplets. It also means that samples collected from animals for bacterial culture and identification should be kept moist and be processed by the laboratory as soon as possible, usually within 24 hours of collection.
Below shows the phylogeny of the Pasteurellaceae.
In this workbook, respiratory diseases of cattle, small ruminants, poultry and pigs will be discussed. Ovine epididymitis will be dealt with in the Chapter on brucellosis and actinobacillosis in the Chapter on abscessation of livestock. Mannheimia haemolytica as a cause of gangrenous mastitis (bluebag) is discussed in Mastitis Chapter.
Less common or less important diseases will only be listed.
Learning Objectives
- Name the important animal pathogens in the Pasteurellaceae, and associate the disease with their natural habitat.
- List the Notifiable bacterial disease in Australia and Australian States and know what the diseases cause and how they are diagnosed (in this Section, it is only haemorrhagic septicaemia).
- Discuss the epidemiology of bovine respiratory disease complex and the pathogenic role of M. haemolytica; P. multocida and H. somni play in this disease.
- Describe the diagnosis of infectious pneumonia in cattle and critically evaluate the sampling methods used.
- Describe the basic principals of the control of BRD in cattle, taking into account the epidemiology, pathogenesis and diagnosis of the causes.
- Discuss the role of the necrotoxins of P. multocida and B. bronchiseptica in the pathogenesis and clinical manifestations of progressive atrophic rhinitis of pigs.
- Compare the pathogenesis, pathology, diagnosis, clinical signs and control of porcine pleuropneumonia and enzootic pneumonia in pigs.
- Be able to diagnose and control bacterial respiratory disease in poultry with special reference to fowl cholera, infectious coryza and avian mycoplasmosis
- Compare the pathogenesis, pathology, diagnosis, clinical signs and control of porcine pleuropneumonia and enzootic pneumonia in pigs.
diseases caused by the Pasteurellaceae
The list of diseases caused by the Pasteurellaceae is long. See Table below. This Family often cause multi-factorial disease syndrome that will vary between animal species. Thus, the important disease syndromes are discussed using an animal species approach. You will also have the opportunity to complete some interactive case studies on some of the respiratory syndromes.
Infections due to Actinobacillus equuli in horses (Sleepy foal disease)
Horses carry A. equuli on the respiratory and external genital mucosae. Originating from the vaginal mucosa of the mare, it is one of the first bacteria to colonise the upper respiratory tract and oral cavity of foals. Thus infections of neonates can occur via the umbilicus, respiratory tract or oral cavity when there is no colostrum derived immunity. The septicaemic disease in neonates is called sleepy foal disease. However, septicaemia in foals can be caused by a number of different bacteria, including Salmonella. Thus bacterial cultures should be carried out on all suspect cases. In adult horses, A. equuli can cause abortions and acute peritonitis. Beta-lactam drugs and potentiated sulphonamides are generally effective treatments, but antimicrobial susceptibility testing should be carried out on cultured isolates.
respiratory disease syndromes in animals
The Pasteurellaceae are involved in a number of respiratory disease syndromes in animals. The ones that will be further discussed are:
- Haemorrhagic septicaemia in ruminants
- Bovine respiratory disease complex (Shipping fever)
- Infectious respiratory disease in small ruminants
- Infectious respiratory and systemic disease in intensively reared pigs
- Infectious upper and lower respiratory tract and systemic disease in intensively reared poultry
Haemorrhagic septicaemia
Haemorrhagic septicaemia (HS) caused by Pasteurella multocida is a major disease of cattle, buffaloes and wild ruminants occurring as catastrophic epizootics in many Asian and African countries, resulting in high mortality (up to 100%) and morbidity (upto 100%). Haemorrhagic septicaemia has never occurred in Oceania, including Australia and is a Notifiable Disease in this country.
The most recent serious epidemics has been recorded leading to 100% deaths in 200 000 Saiga does in Kazakstan in 2015 and Mongolia in 2016. The disease has been recorded in wild mammals in several Asian and European countries. In many Asian countries it is the leading cause of deaths in cattle and buffaloes. Disease outbreaks mostly occur during the climatic conditions typical of monsoon (high humidity and high temperatures). It also occurs when there are great extremes in temperature i.e. cold.
Affected animals have a fever, respiratory distress with nasal discharge, and frothing from the mouth, leading eventually to recumbency and death. Sub-acute cases may show subcutaneous oedema.
Blood smears from affected animals reveal small coccobacilli, with a central pallor. Cultures of fresh blood and organs yield P. multocida, which should then be serotyped. The Asian serotype B:2 and the African serotype E:2 (Carter-Heddleston system), corresponding to 6:B and 6:E (Namioka-Carter system), are mainly responsible for the disease. These strains can also be genotyped.
Bovine respiratory disease complex
Bovine respiratory disease complex (BRD), also called “shipping fever” in cattle is a multifactorial disease. It results from the interaction of stressed young animals with adverse environmental conditions, respiratory viral infections, caused by bovine herpes virus-1 (BHV-1), parainfluenza virus, bovine syncitial virus (BSV) or bovine viral diarrhea virus (BVD), and bacteria belonging to the Family Pasteurellaceae and Mycoplasmoptis spp., (especially Mycoplasmoptis bovis).
Mannheimia haemolytica is usually the cause of up to 70% of acute bronchopneumonia in young cattle. Pasteurella multocida serotype A and Histophilus somni cause sub-acute to chronic bronchopneumonia. Rarely Bibersteinia trehalosi can cause acute bronchopneumonia. Feedlot bronchopneumonia is especially common in the first 42 days that young animals spend in a feedlot.
Bronchopneumonia accounts for 75% disease incidents and 45 to 55% of deaths on a feedlot. Treatment is with antibiotics. It is estimated to cost the feedlot industry about $60 million per annum. It is also second to diarrhoea in causing deaths in calves and is the most common cause of death in live export cattle. BRD accounts for 60% of the cattle deaths on the ships. In 2017 the total mortality rate of cattle during live export was 0.1% (867 of 860 000 cattle or 500 animals to BRD).
Epidemiology of BRD
There are a number of predisposing factors that are interrelated, but all are associated with a young immunologically naive animal that has been subjected to numerous stressors and is at the same time exposed to high levels of infectious agents. Prevention of BRD is based on an understanding of how these factors interrelate and what can be done to minimise any factors that negatively impact on the health of the young beast.
Below is a diagram of a typical pathway of stressors encountered by cattle destined for feedlots or live export. The physiological effects of these stressors is indicated in the Table below.
For more information on the bacterial pathogens of bacterial respiratory disease in feedlot cattle:
The effect of these stressors on the immune system of cattle is shown in the Table below.
The role of the bacterial pathogens, M. haemolytica, P. multocida and H. somni have in the pathogenesis of BRD
Impairment of the pulmonary clearance mechanisms as a consequence of high dust loads, preceding viral, mycoplasmal or bacterial infection and/or stress‑associated factors may allow the bacteria to gain a foothold in the lungs. Mannheimia haemolytica and P. multocida have adhesion fimbriae that attach specifically to respiratory epithelial cells.
Once attached, they will proliferate and produce a number of virulence factors.
Once in the lung, the 3 important bacterial virulence factors are:
- Leucotoxin: Produced during the logarithmic phase of growth of M. haemolytica and Bibersteinia trehalosi it remains confined to the alveolar lumen. Many of the Pasteurellaceae produce pore-forming toxins known as RTX toxins where they bind to CD18 found on leukocytes. This binding is species-specific i.e. the leucotoxin of Mannhemia haemolytica binds specifically to bovine alveolar macrophages, but also neutrophils and platelets. In high concentrations these toxin will lyse the cells they infect. These toxins are also strong antigens and are ideally suited for incorporation as toxoids into vaccines.
- Endotoxin: It is produced by all the gram-negative bacteria and crosses the alveolar wall. It stimulates neutrophil and mast cell activity and degranulation, and damages endothelial cells causing protein flooding of the alveoli and impairing the function of surfactant. The increase in surface tension in the alveoli leads to atelectasis (lung collapse or inability to expand).
- Capsule: Pathogenic strains of P. multocida produce a thick capsule that delays the immune system from recognising them as foreign.
Vasoactive compounds released by predominantly neutrophils results in inflammation with the production of protein-rich inflammatory fluid and capillary thrombosis and subsequently focal coagulative necrosis. Iron is also released from the damaged cells that is grabbed by the bacterial siderophores. The iron then stimulates to growth of the bacteria. The infection can then spread from there to the pleura and heart as well as in the blood to distant organs.
Once in the systemic circulation:
- Endotoxin: Hyper-inflammatory syndrome = endotoxaemia
- Lipooligosaccharides (LOS) on the outer membrane of H. somni attaches to endothelium of arterioles leading to vasculitis. The arterioles of the brain are particularly affected. This can led to the development of thrombotic encephalitis.
- Pasteurella multocida and H. somni are able to persist in the host by surviving intracellularily in phagocytes. They are also able to vary the antigenicity of their LPS by alternating the molecular structure of the O-polysaccharide chains (phase variation)
Diagnosis of bovine respiratory disease (BRD)
The epidemiological (see previous page) and clinical (below) considerations may be sufficient to make a suspected diagnosis of BRD. Post-mortem examinations of cattle that die and abattoir surveillance can assist in determining the severity and prevalence of BRD. Sampling for and identifying the cause and determining antibacterial susceptibilities will assist in a preventative program and the selection of antibiotics for treatment.
Clinical Signs
The disease usually develops within 10-14 days after the animals have been stressed. In peracute cases, or when observation is deficient, animals may simply be found dead. The acute form of the disease is most commonly seen where animals initially develop fever (40-41°C) then a serous nasal discharge and rapid shallow respiration with increased lung sounds. If treated at this stage they respond very well and recover within 24 – 48 hours. Untreated animals become overt clinical cases within a few days and show the following clinical signs:
- Fever
- Listless, head down, ears drooping, stands apart from group
- Congested mucous membranes
- Mucous nasal discharge, becoming mucopurulent
- Weak cough may be present – exacerbated by exercise
- Dyspnoea and increased respiratory rate. Severe cases show both inspiratory and expiratory dyspnoea, often with an expiratory grunt (associated with severe pleuritis) and open-mouth breathing with head and neck extended.
- Auscultation of lungs in the early stages reveals referred bronchial sounds (evidence of congestion and consolidation) over the cranioventral areas which later become louder and more extensive. Crackles, wheezes and sometimes pleuritic friction rubs may be heard in more advanced cases.
- Anorexia, rumen stasis and mild diarrhoea.
- Severe weight loss
Although animals showing these signs mainly recover on treatment, recovery is prolonged. Severe cases, may die or become chronic despite treatment. Although exceptions occur, spontaneous recovery in the absence of treatment is inevitably prolonged and attended by relapses. These animals never do well and are referred to as ‘poor doers’ or ‘pulmonary cripples’.
Samples collected from living animals
- Nasal swabs: Nasal swabs are the easiest samples to collect. However, these are not suitable for the isolation of causative bacteria, as bacterial populations in the nasal cavity are not always representative of those in the lung, even if they are of known pathogenic species. There is severe contamination by commensal bacteria which may impede or prevent the isolation of the causative bacteria.
- Deep nasal swabs: Bit better than nasal swabs, but only 50% of isolates will correlate with that of lower respiratory tract sampling. This is the sample of choice for respiratory viruses as most viruses primarily cause an upper respiratory tract infection. Method: Long sheathed equine uterine swab is passed in through the nostril, exsheathed 20cm deep and swabs the deep nasal and pharyngeal area.
- Tracheal mucus collected by transtracheal aspirate (TTA) or endoscopy. TTAs are the samples of choice as they are usually less contaminated and yield bacteria that are more likely to be the cause of lower respiratory tract disease.(The method is described here to orientate you, but will not be tested as it is essentially BVSc IV coursework – An area of skin covering the ventral aspect of the middle third of the trachea is shaved and sterilised. The trochar part (18G) of an intravenous catheter is passed between two tracheal rings and the flexible part of the catheter is introduced for about 40 cm (up to the entrance of the chest) in the direction of the lung. 50 mL of sterile 0.9% NaCl or pH neutral PBS is lavaged into the lung and retrieved by gentle suction using the syringe. On average, 5–10 mL of fluid should be collected.)
- Bronchoalveolar lavage (BAL). This sampling is done during airway visualisation and samples collected will be representative of the lower respiratory tract airways where the bacteria are causing bronchopneumonia. However, there is some bacterial contamination from the upper respiratory tract of these samples making them less ideal than TTAs.
- Pleural fluid aspiration (thoracocentesis; pleurocentesis): Only do if there is fluid present in the pleural cavity – determined by auscultation, percussion, ultrasound or radiographs. Collected aseptically from the 6th or 7th intercostal spaces below the fluid line on the right hand side. Before carrying out this procedure, revise thoracic anatomy and avoid the blood vessels supplying the ribs.
- Lung biopsies: Important to collect from a consolidated lung area revealed by auscultation, percussion and diagnostic imaging otherwise the lesion may be missed. As this method is done “blindly” there is a risk of haemorrhage. Should be carried out by skilled persons.
Samples collected from dead animals
Note that samples from animals that have died from BRD may reflect treatment failures or bronchopneumonia complicated by opportunistic pathogens. Samples should be collected ASAP after death as many cattle aspirate ruminal contents when dying. Aseptically collected specimens of pneumonic areas and bronchial or mediastinal lymph nodes at necropsy. Select the most caudal portion of the affected lung, as it is less likely to be contaminated. Include the bronchial and mediastinal lymph nodes as they are less likely to be contaminated and are bacterial traps.
Differential diagnosis
When making a diagnosis of bronchopneumonia in cattle, there are a number of causes. Take these into account when requesting laboratory tests. Below are some listed causes.
- Infectious bovine rhinotracheitis (Bovine herpesvirus-1)
- Mycoplasma bovis infections
- Intrapleural or intrapulmonary rupture of a lung abscess (Trueperella pyogenes, Corynebacterium pseudotuberculosis, Burkholderia pseudomallei, Fusobacterium necrophorum),
- Pulmonary embolic aneurysm and interstitial pneumonia.
Other conditions include:
- Foreign‑body or aspiration pneumonia,
- Necrobacillosis (of the upper respiratory tract (rare),
- Salmonellosis
Pathology
Carrying out a post-mortem examination will assist in determining whether bacteria could be the cause of pneumonia in deceased cattle.
- Severe, acute, fibrinous or fibrinonecrotic bronchopneumonia (lobar pneumonia) with fibrinous pleuritis. In addition to the extensive reddish-black to greyish-brown cranioventral consolidation (up to 90 per cent of the lungs below a horizontal line drawn through the dorsal third of the thoracic inlet may be affected) with prominent gelatinous thickening of interlobular septa giving the lung a marbled appearance, areas of coagulation necrosis are a characteristic feature. At their most prominent, they appear as irregular but sharply demarcated regions with thick white boundaries and sunken, deep red, central zones
- Upper respiratory tract is usually only mildly affected. In cases where BHV‑1 infection may have initiated the illness, rhinotracheitis may be particularly severe and extensive with pseudomembranous inflammation predominating
- Fibrinous pericarditis, epi- and endocardial petechiae and ecchymoses, and occasionally, fibrinous peritonitis, polyarthritis and/or meningitis may be present.
- Characteristically at microscopic level “oat cells” are present. Gram-negative bacteria are present in profusion, particularly at the periphery of the necrotic foci, but also in the alveoli and interstitium during the acute stage. (The microscopical features of the lesions may be utilised to stage the pneumonic process: appearance of necrosis at three days, fibroblasts at 4 to 5 days, collagen fibres at 7 days and birefringence of collagen fibres under polarized light at 21 days). – Don’t need to know
Laboratory diagnosis
The laboratory diagnosis is based on the culture and identification of the bacteria, qPCR detecting species-specific DNA/RNA of the viruses. Serotyping of M. haemolytica, B. trehalosi and P. multocida isolates is done using the passive haemagglutination test. It enables one to determine the most predominant serotype in an outbreak and to ensure that this strain is present in the vaccine.
Below is a Table showing the most important identification characteristics of Mannheimia haemolytica, Bibersteinia trehalosi, Pasteurella multocida and Histophilus somni.
Antimicrobial susceptibility testing of the bacterial isolates should be carried out to find out whether there is resistance to commonly used antibiotics. Antibiotics tested include oxytetracycline, penicillin, potentiated sulphonamides, ceftiofur, tilmicosin, tularithromycin and florfenicol.
Control of BRD
Treatment
Early identification of affected animals is the most important single aspect of treatment. If treated early enough, 85-90% of affected cattle will recover within 24 hours. The pens should be worked through twice a day and any sick animals removed, identified and placed in a hospital pen. Good nursing here is extremely important:
- shelter, especially from wind
- sufficient long, good quality grass hay and water available
- reduce concentrates – mix 50:50 with milled roughage
- 18% protein with biological value and NPN, eg. oil cake meal
The choice of antibacterial is dependent on:
- economic considerations
- bacterial susceptibility (resistance may develop with continuous use)
- previous success rate with drug in the same area
- concentration of drug reached in the lungs (usually not a problem due to the inflammation)
Any of the following antibacterials may be effective (know generic name only, link to registered veterinary pharmaceuticals in Australia provided):
- Oxytetracycline (Tetravet; Bivatop)10-20 mg/kg o.i.d. i.m./i.v.
- Potentiated sulphonamides (Tridoxine; Tribactryl; Trisoprim; Terramycin) 1 ml/10 kg o.i.d. i.m./i.v.
- Procaine penicillin 30 000 i.u./kg o.i.d. i.m.
- Ceftiofur (Excenel; Excede, Cefomax, Norocef, Calefur) 1 mg/kg (1 ml/50 kg) o.i.d. i.m.
- Tilmicosin (Mycotil, Timicabs, Tilmix) 10 mg/kg (1 ml/30 kg) once s.c.
- Tularithromycin (Draxxin) 2.5 mg/kg once s.c.
- Florfenicol (Nuflor, AbbeyFlor, Resflor) 20 mg/kg (1 ml/15 kg) q 48 h i.m.
Supportive therapy (often not applicable in feedlot animals)
- Corticosteroids
- NSAIDs
- Support for bactericidal oxidising systems used by alveolar macrophages (don’t learn doses):
Vitamin C 2-4 g o.i.d. i.m. NaI 1 g/15 kg o.i.d. i.v.
- Bronchodilators
Chemoprophylaxis. Antimicrobial agents have been widely used for the prevention of respiratory disease, especially just after arrival in the feedlot. The danger is that chemoprophylaxis can be used to compensate for managemental deficiencies and can result in a false sense of security. Ideally, on arrival those animals exposed to high levels of stress should be identified:
- Excessive shrinkage (>7%). Must weigh group before and after transport.
- If >10% of group have rectal temperatures of ³40°C.
Chemoprophylaxis (metaphylaxis) is then indicated in these groups.
Mass medication can be applied in one or both of the following ways:
- Single injection of long acting oxytetracycline (20 mg/kg i.m.) or other antimicrobial, eg. tilmicosin at processing.
- Antibacterial feed medication. Oxytetracycline at 100 ppm is commonly used. A problem with long-term use is the development of bacterial resistance, therefore it should not be used continuously (eg. use in high risk periods only). (Pasteurella multocida often develops resistance to the tetracyclines and Mycoplasma bovis to the tetracyclines and macrolides)
Prevention
Prevention of BRD depends on two basic principles:
- Reducing stress on the animal
- Increasing the immunity of the animal
Preconditioning, or preparation of the animals for entering the feedlot, involves co-operation between the farmer, feedlot owner and veterinarian. Animals should preferably be acquired directly from the farm of origin rather than from an auction saleyard.
Managemental:
- Dehorning at a few weeks of age.
- Treatment for internal parasites.
- Castration at weaning or earlier.
- Weaning at least 2-3 weeks before admission to feedlot.
- Creep feed at weaning – introduction to feedlot type of feed.
Transport:
- Avoid long distances as much as possible.
- Feed and water available immediately before transport.
- Don’t withhold feed or water for more than 24-30 hours. Reduction in feed and water intake during transport causes “shrinkage”.
- Avoid overcrowding and exposure to exhaust fumes.
Arrival:
- Reception area away from rest of cattle.
- Fresh water and long hay available.
- 50:50 concentrate:roughage ratio. 18% protein with biological value and NPN.
- Provide additional potassium (1,5% of ration) with concentrate (K+ levels rapidly depleted in cattle which haven’t eaten for 2-3 days)
- Processing should take place soon after arrival (within 24 hours).
- Vaccination against respiratory viruses is usually done for the first time on arrival. This is of questionable value since most animals seroconvert shortly after arrival anyway.
- Mixing of cattle from different sources should be avoided in order to minimize stress and reduce the potential for cross-infection
- Animals of similar size, type and gender should be penned together, and the pen population should be held at below 200 head.
- Handling of recent arrivals, except for processing, should be curtailed for at least 21 days.
- Feed and manure dust control by adjusting the water, molasses and fat content of the ration. Water sprinkling systems and regular removal schedules are the predominant means of dust control during periods of high environmental loads.
- Protect against wind chill (wind breaks)
Vaccination
It is common practice to vaccinate calves against the viruses that predispose to bacterial bronchopneumonia. This should ideally be done at least 2-3 weeks before transport to the feedlot. A booster may then be given on arrival. Vaccination against M. haemolytica should also be done at the same time.
Vaccination against M. haemolytica: Although antibodies to capsular components (opsonising antibodies) may play a role in immunity, it is antibodies to leukotoxin that are far more important. The presence of antibodies to capsular components only, may result in increased severity of pneumonia due to enhanced bacterial-induced macrophage cytotoxicity. Leukotoxin toxoids produce only anti-leukotoxin antibodies. The current bacterin-toxoid vaccines do both (Live vaccines, however, will stimulate production of anti-leukotoxin as well as anti-capsule antibodies – none registered in Australia).
Vaccines currently available in Australia (viral and/or bacterial): (don’t need to know)
Inactivated vaccines:
- Coopers Bovilis MH Mannheimia haemolytica vaccine for cattle leucotoxin strain x332 / inactivated Mannheimia haemolytica strain x387 polymyxin B sulfate / thiomersal
- Coopers bovilis MH + IBR bovine respiratory disease (brd) vaccine inactivated bovine herpes virus type 1.2b / inactivated Mannheimia haemolytica strain x387
- Zoetis Bovishield MH One containing inactivated M. haemolytica NL1009 (leukotoxin and capsular antigen) – one dose 14 days prior to shipping.
- Coopers bovilis IBR infectious bovine rhinotracheitis (IBR) vaccine for cattle inactivated bovine herpes virus type 1.2b
- Zoetis Pestiguard contains inactivated Pestivirus – only vaccinate on farm as this vaccine can be immunosuppressive in stressed livestock.
Live vaccine:
- Rhinogard bovine herpesvirus 1 live intranasal liquid vaccine for feedlot cattle bovine herpesvirus 1
Infectious respiratory disease in small ruminants
Pasteurella multocida or Mannheimia haemolytica is the cause of bronchopneumonia and a fibrinous pleuritis in stressed lambs and kids. Respiratory infections are usually a complication of infections with respiratory viruses or mycoplasmas. Bibersteinia (formerly Pasteurella) trehalosi is the cause of septicaemia in lambs. Fever, anorexia, coughing, a nasal discharge and respiratory distress usually occurs 10 to 14 days after the stress. The pathology resembles that that occurs in bronchopneumonia of feedlot cattle. Treatment and control is the same as for feedlot cattle. (Read the section on Bovine respiratory disease).
Infectious respiratory and systemic disease in intensively reared pigs
Three respiratory syndromes associated with bacterial infections are commonly recognised in pigs. They are:
- Atropic rhinitis. Only progressive atropic rhinitis is of economical importance.
- Porcine pleuropneumonia (Actinobacillus pleuropneumoniae – APP)
- Mycoplasma pneumonia/enzootic pneumonia of pigs caused by Mesomycoplasma hyopneumoniae
- Pasteurellosis in pigs caused by Pasteurella multocida
- Glasser’s disease a polyserositis caused by Glasserella parasuis
1.Progressive atrophic rhinitis
Progressive atrophic rhinitis is a chronic debilitating contagious disease of the upper respiratory tract in pigs from 3 to 6 weeks of age and is caused by necrotoxin-positive Pasteurella multocida (serovars A and D) and Bordetella bronchiseptica (a gram-negative non-fermentative bacterium). The exotoxins induce inflammation of the nasal mucosae as well as bone remodelling (osteoclast activation) resulting in sneezing and snout shortening and deviations. The lacrimal ducts are often occluded resulting in tear staining of the cheeks. The introduction of carrier pigs suffering from concurrent disease as well as overcrowded conditions and poor ventilation contribute to the severity of disease. Disease is more common when the parity distribution of the sow herd is low – young sow herd. This is because young sows shed more bacteria and produce less lactigenic immunity for their piglets than older sows. The disease is diagnosed by the detection of toxigenic P. multocida on the nasal mucosa. This can be done by PCR or to improve the test sensitivity by culture followed by PCR identification of the toxin encoding gene.
Routine monitoring of herds is done by snout scoring at the abattoir. The snout is transected at the level of the 2nd premolar and the degree of nasal septum deviation and turbinate atrophy is scored from 0 (none) to 5 (marked nasal septum deviation and loss of most of the turbinates).
Usually a low level of atrophic rhinitis is tolerated in a herd. Should the disease prevalence get high antibiotics such as tylosin, tetracycline, ceftiofur and sulphonamides are administered to the sows, the sucklers and weaners. (Immunsation with a bacterin-toxoid mixture of P. multocida and B. bronchiseptica has proven to be effective in reducing the manifestation of disease – not available in Australia).
Non-progressive atrophic rhinitis is caused by B. bronchiseptica is a mild disease and is not usually treated or controlled.
2.Porcine pleuropneumonia (Actinobacillus pleuropneumoniae – APP)
Porcine pleuropneumonia of swine is an infectious porcine respiratory disease caused by Actinobacillus pleuropneumoniae that results in severe economic losses worldwide in the swine industry. These marked economic losses are associated with retardation in the growth of infected pigs. This disease should be distinguished from Mycoplasma pneumonia in swine caused by Mycoplasma hyopneumoniae (a bacterium that does not have an outer membrane). (It is discussed in the following paragraph)
The bacterium is spread by nose to nose contact or limited droplet inhalation. When carrier pigs, usually gilts, are introduced into a “clean” herd, the onset of clinical signs is sudden and develops within 4 to 12 hours after infection causing peracture disease. A marked drop in environmental temperature can precipitate an outbreak. Some pigs may be found dead, whilst others will have a fever and exhibit extreme respiratory distress. The lungs typically show a pleuropneumonia and blood and froth are found in the trachea. The disease is often complicated by concurrent P. multocida infections. Once the disease is endemic sub-acute and chronic forms of porcine pleuropneumonia are more common. Recovered pigs or those with partial immunity may develop the chronic form of the disease where they become “poor-doers” and develop a persistent cough.
The pneumonic lesions in pigs are associated with the porin exotoxins APX I, APX II, APX III and APXIV which act synergistically (mainly APXI and APX II) to lyse alveolar epithelium, macrophages, neutrophils and erythrocytes. Endotoxin is also produced.
Although the distribution of the lesions at the abattoir is variable, most lesions are found in the dorso-caudal area where they are palpated as firm nodules. Fibrinous and fibrous adhesions are found on the pleural surfaces. When transected these nodules are well encapsulated “sequestra”. APP is best diagnosed by culture of the bacterium from the most caudal lesions (least contaminated).The bacterium is typical of the Pasteurellaceae, in that it is a gram-negative coccobacillus, non-motile and fermentative. However, it is V-factor dependent, beta-haemolytic and produces urease. 15 different capsule serotypes are recognised: Serotypes 1, 2, 5, 9 and 11 are considered virulent isolates, being responsible for either acute or chronic outbreaks of APP.
Usually antibiotics such as ceftiofur, tetracyclines, synthetic penicillins, tylosin, and potentiated sulfonamides are required to treat an outbreak of the disease. The disease can be controlled in endemic herds by segregated early weaning, “all-in-all-out” management, reduced stocking rate, and improved ventilation. Bacterin vaccines are effective in areas that are infected with the serotype present in the vaccine i.e. 1, 7 and 15. Autogenous vaccines can be used on farms where the infecting serotype has been identified. Where the disease is severe, farms have eradicated APP by depopulating the farm and then repopulating the farm with A. pleuropneumoniae–free stock. Serologic testing and lung scoring at the abattoir should be carried out routinely on these farms to monitor for infection and disease.
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Mycoplasmal pneumonia/enzootic pneumonia of pigs caused by Mesomycoplasma hyopneumoniae
(This disease is dealt with in this section as it is a predisposing factor for the other bacterial infections of the respiratory tract, and most of the control measures used are common for all the respiratory tract infections)
Mycoplasma pneumonia is a chronic, low grade, contagious pneumonia of pigs caused by Mesomycoplasma (former Mycoplasma) hyopneumoniae. Affected pigs have a persistent soft cough especially when roused and retarded growth rates. The disease in well managed pig units is often subclinical or mild. A severe pneumonia can develop when there are breakdowns in management, concurrent viral infections, when there has been a sudden change in weather, or when the disease is newly introduced into a herd. This is because the respiratory tract becomes secondarily infected with Pasteurella multocida, Actinobacillus pleuropneumoniae, Glaesserella parasuis or Streptococcus suis.
Bacteria are usually transmitted from the sow in respiratory droplets to her offspring. Pigs also become infected when they are introduced post-weaning or at an older age i.e. replacement gilts to other infected pigs. Mycoplasmas colonise the upper respiratory tract where they destroy the respiratory cilia. The virulence of these bacteria are enhanced by respiratory viruses and other mycoplasmas such as Mesomycoplasma hyorhinis. Since the outer surface of the bacteria is antigenically similar to respiratory cell surfaces, immunity is slow to develop. However, when it does, there is a strong inflammatory response which leads to tissue destruction. Thus disease is often only evident at 3 to 5 months of age. Thus lung lesions are typically seen at the meatworks. The damage to the cilia and inflammation allow secondary bacterial infections.
The apical and cardiac lobes are commonly affected where they are sunken, gray or purple. Old lesions become clearly demarcated. The associated lymph nodes may be enlarged.
A suspect diagnosis is made based on a history of coughing and the lung lesion distribution. The lung is typically scored at the meatworks with a higher score given to more cranial lesions and more extensive lesions (see picture below). The bacteria can be cultured, but requires very fresh lung and lymph nodes samples and special media. Cut sections of affected lung can be used for immunohistochemistry: immunofluorescence of immunoperoxidase test – where monoclonal antibodies are used to detect M. hyopneumoniae . A qPCR can detect M. hyopneumonniae DNA in nasal fluids and lungs.
Disease control
- During an outbreak antibiotics: tiamulin or tetracyclines can be used to reduce evidence of disease.
- Management procedures such as improving the ventillation, reducing the stocking density and making use of an all-in-all-out systems can reduce the effect of disease.
- New pigs should be quarantined for at least 6 weeks and be kept 1 km from the other pigs.
- Depopulation and then repopulation with disease-free pigs may work in Australia as the climate is dry, mostly warm and there is a low density of pig farms (> 3 km apart). In Europe where there is a moist, cold climate with a high density of pig farms, inter-farm transmission of the mycoplasmas occurs.
- Some farms have used with success a partial depopulation program, where animals most likely to shed mycoplasmas are sent to the meatworks and older with a solid immunity are retained and treated for two weeks with tiamulin. Breakdowns in disease have also occured on farms that have used segregated early weaning and PCR negative pigs for breeding. The main reason being is that the tracheal cilia can be colonised early and not all positive pigs are detected with PCR.
- Vaccinate piglets with bacterins as it can decrease the disease prevalence. Prefarrowing vaccination of sows reduces her shedding bacteria and provide passive immunity.
4.Pasteurellosis in pigs caused by Pasteurella multocida
Lungs already infected with Mesomycoplasma hyopneumonia (enzootic pneumonia) or Actinobacillus pleuropneumoniae are susceptible to super-infections with Pasteurella multocida serotype A (non-toxigenic strains). This results in an exudative bronchopneumonia, sometimes accompanied by a fibrinous pleuritis and polyarthritis. Primary lung lesions due to P. multocida are uncommon.
This disease is controlled by aggressive antibiotic therapy. Of the Pasteurellaceae, P. multocida is most likely to develop antibiotic resistance, so it is important that it be cultured from the lungs of affected pigs on farms where chemoprophylaxis is practiced. This disease is best prevented by controlling the primary bacterial causes i.e. Mesomycoplasma hyopneumoniae.
5. Glasser’s disease a polyserositis caused by Glasserella parasuis
Glasser’s disease is a sporadically occurring infectious polyserositis of 3 week to 4 month old pigs caused by the V-factor dependent Glaesserella (formerly Haemophilus) parasuis. This is a signficant disease of age-segregated management systems globally.
Glaesserella parasuis is part of the normal nasopharyngeal microflora. Nursing piglets are infected by their mother by droplet transmission from birth, but show no clinical signs during the period of passive immunity. Disease only develops if the piglets are stressed or there is a concurrent viral or bacterial infection. Glasser’s disease is more common in regions where PRRSV (porcine respiratory and reproductive syndrome virus) is present. Once the bacteria establishes itself, it distributes throught the body targeting multiple serosal surfaces and the brain. It can also cause secondary infections of the lung. At the localisation sites, it stimulates a vasculitis and an inflammatory response.
Clinical signs occur suddenly with the best pigs being affected. There is a low morbidity, but a high mortality rate. Pigs may be found dead or die within 2 days. After an initial fever, clinical signs are associated with the site of localisation. Nervous signs are the most common with tremours, incoordination, posterior paresis and lateral recumbency; lameness due to multiple joints being affected; evidence of septicaemia and respiratory disease may also be present. Chronically affected animals show growth retardation.
Serofibrinous or fibrinopurulent exudate may be present in the peritoneal cavity, thoracic cavity, pericardial sac, various joints and on the brain. Serosal surfaces appear rough due to the presence of a fibrin.
Since this disease can resemble other diseases including infections caused by Streptococcus suis and Actinobacillus suis, it should be cultured and identified. Note that fresh samples are required to culture this very delicate and nutritionally fastidious bacterium.
Management of the disease is based upon antibiotic treatment of sick animals or animals at risk, good husbandry aimed at reducing stress and other respiratory tract infections. Penicillin is effective against this bacterium. Since the piglets are infected so early in life, segregated rearing is less effective. Bacterin vaccines have been developed but are often ineffective as there are at least 21 serovars and many untypeable strains that can infect pigs and they are poorly cross-protective. In situations where high numbers of pigs are affected, it may be valuable to make use of autogenous vaccines. Another method of control is to expose nursing piglets with protective passive immunity to small amounts of the serovar of H. parasuis that is common to the farm.
Registered vaccines in Australia for respiratory disease in pigs is listed below (you don’t need to know them)
- Merck M+Pac® Mycoplasma hyopneumoniae inactivated vaccine for pigs (J strain) administered at 7 days and then 6 weeks of age.
- Zoetis RespiSure® One Single dose bacterin of M. hyopneumoniae administered at 3 weeks, but can be administered at 1 day of age.
- Ingelvac MycoFLEX® Injection bacterin from 3 weeks of age
- Porcilis APPvac pleuropneumonia vaccine for pigs Actinobacillus pleuropneumoniae serovars 1, 7, 15, haemolysin toxoid APXI, APXII and APXIII.
- Ausvac PLEURAVAC pleuropneumonia Vaccine for Pigs Inactivated adjuvanted bacterin and toxoid.
infectious respiratory disease in birds with special reference to poultry
Like in cattle and pigs, avian respiratory disease complex in stressed birds is caused by a complex interaction between the environment and respiratory viral and bacterial pathogens.
- Environment: Aerosol-rich environment; high ammonia levels; heat or cold stress; high animal density; mycotoxins present in food and bedding
- Immuosuppressive viruses: IBD, IA, MD, Reovirus
- Respiratory viruses: ND, IB, AI, LTV, NV
- Primary bacterial pathogens – Pasteurella multocida (fowl typhoid), Avibacterium paragallinarum (infectious coryza) and Mycoplasmoides gallisepticum (avian mycoplasmosis)
- Opportunistic bacteria – Gallibacterium anatis, Ornithobacterium rhinotracheale (not diagnosed in Australia, but present world-wide including New Zealand), Escherichia coli
Bacterial respiratory diseases of importance in poultry, include:
- Fowl cholera caused by Pasteurella multocida
- Infectious coryza caused by Avibacterium paragallinarum
- Avian mycoplasmosis caused by Mycoplasmoides gallisepticum
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Fowl cholera caused by Pasteurella multocida
Fowl cholera caused by Pasteurella multocida capsular types A, B, D and F is a fatal septicaemia common in all poultry and water birds. Adult birds, especially layers, are highly susceptible. The disease is more common in cold and wet weather or when the birds are heat-stressed. Infected new birds, wild birds or rodents who have eaten infected carcasses on a neighbouring farm will introduce the disease. Chronically infected carrier birds will maintain the disease in a flock. Transmission is by ingestion or droplet inhalation from bird droppings or beak and choanae excretions.
The pathogenesis of P. multocida is similar to that in cattle:
- Fimbriae: adhesions
- A capsule that resists phagocytosis and complement-mediated immune lysis
- Endotoxin: inflammation
In susceptible birds deaths occur 6 to 12 hours after infection. Acute infection is characterised by a green diarrhoea and swollen wattles. Localised infections of the respiratory tract, sinuses of the head, ears, bones, hock joints, sternal bursa, foot pads, peritoneal cavity and oviducts occur.
Post-mortem examination reveals petechiae in the epicardial fatty tissue and necrotic foci in the liver. Necrotic lesions can be present in the respiratory tract and other organs of the body. Due to the speed of infection and mortality, birds are in good body condition and do not exhibit the signs of prolonged illness.
Note that this disease is similar to that caused by Riemerella anatipestifer (not in Australia),S almonella and E. coli
Diagnosis is by the culture of P. multocida from lesions.
Control of fowl cholera
The most efficient treatment in breeding flocks or laying hens is individual intramuscular injections of a long-acting tetracyclines, with the same antibiotic in drinking water, simultaneously. The mortality and clinical signs will stop within one week. Early infections can be treated with penicillins. Potentiated sulphonamides should only be used in non-laying birds.
Sanitation practices for prevention include:
- Complete depopulation each year with a definite break between older birds and their replacements. (All-in-all-out farming system)
- A good rodent control program.
- Proper disposal of dead birds.
- A safe, sanitary water supply.
- Adequate cleaning and disinfection of all houses and equipment on premises where outbreaks have occurred after disposal of affected flocks.
- If housed on soil – allowing contaminated areas to remain vacant for at least 3 months.
Vaccination (Just know that there are vaccines). Those registered in Australia are:
- Bacterin vaccines: Poulvac®I or Pabac® IV
- Live-attentuated vaccine: Vaxsafe®PM containing Pasteurella multocida strain pmp-1
2.Infectious coryza caused by Avibacterium paragallinarum
Infectious Coryza is a contagious bacterial disease of the sinuses of the head and upper respiratory tract and is caused by Avibacterium (formerly Haemophilus) paragallinarum. Most strains require V-factor (NAD-dependent) for growth and are catalase-negative. Satellite colonies grow only in area of blood agar that has been haemolysed by Staphylococcus aureus haemolysins. A. paragallinarum strains are grouped into A, B and C serovars.
Sub-clinical carrier birds introduce it into a flock, where in susceptible birds it causes facial oedema, conjunctivitis, and a brownish nasal discharge 1 to 3 days after infection. The disease occurs in all age groups, but is more common in pullets and layers where it can cause up to a 30% drop in egg production. Stress, overcrowding and concurrent disease (i.e. mycoplasmosis) increase the severity and prolongs the course of disease.
Other agents causing similar disease include P. multocida (fowl cholera), Ornithobacterium rhinotracheale a gram-negative, non-fermentative rod and Mycoplasmoides gallisepticum (avian mycoplasmosis) and viral diseases such as avian pnemovirus with E. coli (swollen head syndrome), laryngotracheitis, infectious bronchitis, avian influenza and Newcastle disease.
Diagnosis is either by culture of the bacterium followed by serotyping or by qPCR.
Treat the disease by mass medication of water using the macrolides (erythromycin, tylosin) or tetracyclines. Although potentiated sulphonamides are effective, don’t use them in layers. Infectious coryza is prevented by preventing contact between susceptible and infected birds i.e. ensuring that only disease-free stock is introduced into clean flocks, by not mixing age groups and an all-in, all-out farming system.
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