bovine parainfluenza 3 infection
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IdentityTop of page
Preferred Scientific Name
- bovine parainfluenza 3 infection
International Common Names
- English: bovine respiratory disease; bovine respiratory disease caused by BPIV 3; enzootic pneumonia of calves; parainfluenza virus, pi-3, infection in sheep and goats; shipping fever; shipping fever of cattle; undifferentiated respiratory disease of cattle
- Chinese: xin fu nian liu gan bing du
OverviewTop of page
Bovine parainfluenza virus 3 (BPIV3) is an important pathogen that causes acute upper and lower respiratory tract infections in calves (Bryson et al., 1978). The virus was isolated for the first time in 1959 from mucus of a calf with respiratory disease and was identified as a myxovirus (Reisinger et al., 1959). Since that time, BPIV3 has been frequently associated with outbreaks of respiratory disease in dairy and beef calves in many countries (Betts et al., 1964; Tsai and Thomson, 1975; Allan et al., 1978; Bryson et al., 1978, 1979a, b). Subsequently, pneumonia typical of field cases was reproduced experimentally by infecting calves with BPIV3 (Tsai and Thomson, 1975; Bryson et al., 1979a, b). In the acute phase of the pneumonia, virus replication was observed within epithelial cells of the respiratory tract and within alveolar macrophages, and loss of cilia and ciliated cells in bronchi and broncheoli and necrosis of bronchiolar epithelium was noted (Tsai and Thomson, 1975; Bryson et al., 1983).
Although an infection with BPIV3 may cause pathology in the respiratory tract of young cattle, this is often subclinical and generally not associated with a recognizable clinical syndrome. The true impact of a BPIV3 infection is that, by causing damage to cells of the respiratory tract, it can impair pulmonary clearance from the lung and predispose calves to secondary infections by other pathogens. As such, BPIV3 is associated with respiratory disease, a major cause of morbidity and mortality in dairy and veal calves (enzootic pneumonia) and feedlot calves (shipping fever pneumonia) that results in substantial economic losses (Thomson, 1980; Yates, 1980; Ghram et al., 1989; Anon., 1992; Radostits et al., 2000a,b). Factors associated with the etiology of bovine respiratory disease are viruses (BPIV3, bovine herpesvirus 1, bovine viral diarrhoea virus, bovine respiratory syncytial virus), bacteria (Mannheimia [Pasteurella] haemolytica, Pasteurella multocida and Haemophilus somnus [Histophilus somni]), stress, and management practices (Yates, 1980; Rebhun et al., 1995; Otter and Farrer, 1997; Radostits et al., 2000a,b). Frequently, more than one infectious agent is involved and together they may act in synergy (Rosenquist et al., 1970; Irwin et al., 1979; Yates, 1980; Ghram et al., 1989).
BPIV3 is an enveloped, non-segmented, negative-sense, single-stranded RNA virus classified in the genus Respirovirus in the Paramyxoviridae family, order Mononegavirales (King et al., 2012).
The Paramyxoviridae contains important pathogens of humans (measles virus, human respiratory syncytial virus, human parainfluenza virus 3 and mumps), and livestock and poultry (bovine parainfluenza virus 3, bovine respiratory syncytial virus, rinderpest virus and Newcastle disease virus; Murphy, 1996), as well as the virus of canine distemper.
Hosts/Species AffectedTop of page
Parainfluenza viruses generally have a narrow host range (Murphy, 1996). The natural host for BPIV3 is cattle. Based on serology, antibodies to PIV3 have been found in humans, cattle, sheep, goats, water buffalo, deer, dogs, cats, monkeys, guineapigs, pigs, and rats (Tehteh and Goyal, 1988; Maglione and Rosati, 1988; Ulbrich, 1991; Fenner et al., 1993; Aguirre et al., 1995). Although there is a serological relationship, it is not clear whether BPIV3 infects all of these species under natural circumstances or whether there are species-specific virus strains. Human PIV3 (HPIV3) is serologically and antigenically different from BPIV3 (Andrewes et al., 1978; Klippmark et al., 1990). BPIV3 can infect humans, sheep, goats, and bisons, but is probably not pathogenic in these species (Rodger, 1989; Zarnke and Erickson, 1990; Bechmann, 1997). Vaccines using BPIV3 have been used to vaccinate humans and sheep and were found to be safe (Karron et al., 1995). It is not known if PIV3 viruses of other species can infect cattle. PIV3 can cause a mild undifferentiated pneumonia in sheep and goats, and surveys have shown that PIV3 infections are widespread and are associated with respiratory disease of economical importance (Martin, 1996; Watt, 1996). Infections in sheep and goats causing disease are probably caused by species-specific PIV3 isolates.
DistributionTop of page
Reports on serological surveys and virus isolations demonstrate that BPIV3 has a worldwide geographical distribution. Seroprevalence is generally high and varies from 50 to 90% (Fenner et al., 1993; Martin, 1996; Radostits et al., 2000a,b).
The complete genome analyses of the representative BPIV3 isolates from Australia and North America indicated that BPIV3 falls into two distinct genotypes, BPIV3 genotype A (BPIV-3a) and BPIV3 genotype B (BPIV-3b) (Horwood et al., 2008). Four isolates, which were only detected in China, were proposed as genotype C (Zhu et al., 2011).
Distribution TableTop of page
The distribution in this summary table is based on all the information available. When several references are cited, they may give conflicting information on the status. Further details may be available for individual references in the Distribution Table Details section which can be selected by going to Generate Report.
|Continent/Country/Region||Distribution||Last Reported||Origin||First Reported||Invasive||Reference||Notes|
|China||Widespread||Zhu et al., 2011; Wen et al., 2012; Wang et al., 2014|
|Indonesia||Widespread||Itoh et al., 1989|
|Iran||Present||Ezzi et al., 2013; Farzinpour et al., 2014|
|Japan||Widespread||Komoda et al., 1988; Kadoi et al., 1998|
|Korea, Republic of||Widespread||Kim et al., 1988|
|-Russia (Asia)||Widespread||Zhumabaev and Belousova, 1992; Masimov, 1994|
|Saudi Arabia||Present||Mahmoud and Allam, 2013|
|Syria||Widespread||Tabbaa, 1989; Giangaspero et al., 1992|
|Taiwan||Widespread||Liao et al., 1992|
|Thailand||Widespread||Virakul et al., 1997|
|Turkey||Widespread||Oztürk and Yavru, 1988; Oztürk and Duman, 1992; Ozdarendeli et al., 1997|
|Congo Democratic Republic||Widespread||Jetteur et al., 1988|
|Egypt||Widespread||Wassel et al., 1996|
|Mali||Widespread||Maiga and Sarr, 1992|
|Nigeria||Widespread||Ibu et al., 1996|
|South Africa||Widespread||Odendaal et al., 1997|
|Tunisia||Widespread||Ghram and Minocha, 1990|
|Canada||Widespread||Ettinger and Feldman, 2000|
|-Alberta||Widespread||Durham and Hassard, 1990|
|-Ontario||Widespread||Martin and Bohac, 1986; Martin et al., 1989|
|-Saskatchewan||Widespread||Durham and Hassard, 1990; Donkersgoed et al., 1993|
|Mexico||Widespread||Melgarejo et al., 1991|
|USA||Widespread||Anon., 1992; Fulton et al., 2000|
|Argentina||Widespread||Ruiz et al., 1989; Fulton et al., 2000; Maidana et al., 2012|
|Brazil||Widespread||Dal et al., 1989|
|Chile||Widespread||Riedemann et al., 1996|
|Colombia||Present||Betancur et al., 2010|
|Peru||Present||Solís et al., 2010|
|Albania||Widespread||Ikonomi et al., 1988|
|Belarus||Localised||Muzychin and Letetskii, 1988|
|Belgium||Present||Pardon et al., 2011|
|Bulgaria||Localised||Kosarov et al., 1998|
|Croatia||Localised||Ledinek and Silak, 1995|
|Czech Republic||Localised||Trávnícek, 1999|
|Denmark||Widespread||Tegtmeier et al., 1999|
|France||Widespread||Penn and Savey, 1990|
|Germany||Widespread||Senf et al., 1988|
|Greece||Widespread||Kakamoukas et al., 1989|
|Hungary||Widespread||Rusvai and Fodor, 1998; Miklós et al., 1999|
|Ireland||Widespread||Healy et al., 1993|
|Italy||Widespread||Maglione and Rosati, 1988; Moriconi and Gnaccarini, 1991|
|Lithuania||Present||Kestaitiene et al., 2009|
|Netherlands||Widespread||Verhoeff and Nieuwstadt, 1984|
|Norway||Present||Gulliksen et al., 2009|
|Poland||Widespread||Klimentowski et al., 1995|
|Romania||Widespread||Cambir and Coman, 1991|
|Russian Federation||Present||Present based on regional distribution.|
|-Russia (Europe)||Widespread||Zhumabaev and Belousova, 1992; Masimov, 1994|
|-Southern Russia||Widespread||Zhumabaev and Belousova, 1992|
|Slovakia||Widespread||Kovác et al., 1995|
|Spain||Widespread||Catalán et al., 1994|
|Switzerland||Widespread||Läuchli et al., 1990|
|UK||Widespread||Stott et al., 1980|
|Ukraine||Widespread||Stetsenko et al., 1992|
|Yugoslavia (former)||Localised||Vinkovic and Cac, 1990|
|Yugoslavia (Serbia and Montenegro)||Localised||Lazic et al., 1995|
|Australia||Widespread||Dunn et al., 1998|
|New Zealand||Widespread||Motha et al., 1997; Motha and Hansen, 1998|
PathologyTop of page
Pneumonia caused by BPIV3 by itself is usually subclinical. Necropsy findings in the apical and cardiac lobes consist of areas of atelectasis and emphysema. In the later stages of infection, dark red-coloured consolidations on apical and cardiac lobes are observed. Bronchointerstitial pneumonia is observed histologically. Generally, an acute inflammation of the nasal mucosa is accompanied by mucopurulent exudate. Microscopically, there are lesions consisting of bronchiolitis, bronchial and bronchiolar hyperplasia, alveolar epithelialization, and giant cell or syncytial formation (Radostits et al., 2000a).
DiagnosisTop of page
The clinical signs of BPIV3 infection in calves or cattle are generally not specific enough to lead to a definitive diagnosis. Therefore, a diagnosis of a BPIV3 infection is based on recovery of the virus from animal samples or on demonstration of an increase in BPIV3 antibody titres in paired serum samples in the laboratory. Samples obtained via tracheal wash, nasopharyngeal swab, or necropsy specimens from infected calves are inoculated in cell culture. Virus is allowed to replicate in cell culture and identified by immunological staining using BPIV3-specific antibodies (Haanes et al., 1997). A direct analysis for BPIV3 can be performed on specimens taken from the respiratory tract, including specimens collected from fatal cases followed by an identification of viral antigens using immunological detection (Gardner et al., 1971; Haines et al., 1992). Alternatively, virus can be assayed by screening for viral RNA in nasal secretions by reverse transcription followed by PCR and immunodetection (Karron et al., 1994). In general, BPIV3 is only detected during the first 7-8 days after infection and is often absent in specimens taken during secondary bacterial infections. Serological diagnosis of BPIV3 antibodies in paired serum samples by complement fixation (CF), haemagglutination inhibition (HI), virus neutralization (VN), or ELISA can establish the occurrence of a virus infection (Assaf et al., 1983; Trybala et al., 1989; van Donkersgoed et al., 1991; Graham et al., 1999).
Because of the multifactorial aetiology of bovine respiratory disease (shipping fever), the high incidence of subclinical BPIV3 infections and the use of modified live virus BPIV3 vaccines, detecting the virus, viral antigens or viral nucleic acid does not prove disease causation. Therefore, the test results should be interpreted after taking into consideration the overall clinical condition of the herd and the individual animal (MacLachlan and Dubovi, 2011).
List of Symptoms/SignsTop of page
|Digestive Signs / Anorexia, loss or decreased appetite, not nursing, off feed||Cattle & Buffaloes:Calf||Sign|
|General Signs / Exercise intolerance, tires easily||Cattle & Buffaloes:Calf||Sign|
|General Signs / Fever, pyrexia, hyperthermia||Cattle & Buffaloes:Calf||Sign|
|Nervous Signs / Dullness, depression, lethargy, depressed, lethargic, listless||Cattle & Buffaloes:Calf||Sign|
|Ophthalmology Signs / Lacrimation, tearing, serous ocular discharge, watery eyes||Sign|
|Pain / Discomfort Signs / Pain, pharynx, larynx, trachea||Cattle & Buffaloes:Calf||Sign|
|Reproductive Signs / Abortion or weak newborns, stillbirth||Cattle & Buffaloes:Calf,Cattle & Buffaloes:Heifer,Cattle & Buffaloes:Cow||Sign|
|Respiratory Signs / Abnormal breathing sounds of the upper airway, airflow obstruction, stertor, snoring||Cattle & Buffaloes:Calf||Sign|
|Respiratory Signs / Abnormal lung or pleural sounds, rales, crackles, wheezes, friction rubs||Cattle & Buffaloes:Calf||Sign|
|Respiratory Signs / Coughing, coughs||Cattle & Buffaloes:Calf||Sign|
|Respiratory Signs / Dyspnea, difficult, open mouth breathing, grunt, gasping||Sign|
|Respiratory Signs / Increased respiratory rate, polypnea, tachypnea, hyperpnea||Cattle & Buffaloes:Calf||Sign|
|Respiratory Signs / Mucoid nasal discharge, serous, watery||Cattle & Buffaloes:Calf||Sign|
|Respiratory Signs / Nasal mucosal ulcers, vesicles, erosions, cuts, tears, papules, pustules||Sign|
Disease CourseTop of page
Young cattle usually become susceptible to BPIV3 infection when maternal antibody levels are dropping. The clinical signs of a BPIV3 infection include fever of 40-41.7°C, depression, anorexia, nasal and ocular serous discharge, increased respiratory rate (40-80/min) tracheal rales, and occasional rales in the lower parts of the lung. Recovery from acute infection is usually within 7-10 days (Bryson et al., 1979a, b). Fatal cases due to BPIV3 infection by itself are rare. A BPIV3 infection can cause lesions in the ciliated epithelial lining of the respiratory tract and BPIV3 can infect alveolar macrophages and hence impair the defence mechanisms against respiratory pathogens (Liggitt et al., 1985; Slauson et al., 1987; Brown and Ananaba, 1988; Basaraba et al., 1993). Therefore, in most cases of a moderate to severe (including fatal) pneumonia, a BPIV3 infection is usually accompanied by bacterial infection. The most common bacteria encountered in complicated pneumonia are Mannheimia [Pasteurella] haemolytica, Pasteurella multocida and Haemophilus somnus [Histophilus somni] (Otter and Farrer, 1997; Radostits et al., 2000a, b).
EpidemiologyTop of page
The prevalence of BPIV3-specific antibodies in dairy and beef cattle is high and the virus is commonly isolated from calves with respiratory disease (Potgieter, 1977; Thomson, 1980; Fulton et al., 1982; Key and Derbyshire, 1984; Martin and Bohac, 1986; Radostits et al., 2000a,b). A BPIV3 infection of calves is generally subclinical in the absence of other pathogens and adverse environmental and management factors (Rebhun et al., 1995; Radostits et al., 2000a,b). An uncomplicated respiratory infection caused by BPIV3 is characterized by clinical signs for 3-5 days followed by a complete recovery (Fenner et al., 1993). Usually, housed dairy calves and nursing beef calves become infected with BPIV3 when they are 1-5 months old. Beef calves often become infected within 2 weeks when they enter a feedlot. Following BPIV3 infection, virus can be isolated for 1-2 weeks from individual calves and can persist for several weeks in the group. By interference with the pulmonary clearance system the virus is capable of predisposing infected young calves to more severe pneumonia (enzootic pneumonia and shipping fever pneumonia) when they are subsequently exposed to bacterial pathogens such as Mannheimia [Pasteurella] haemolytica (Radostits et al., 2000a,b). A combined infection with BPIV3 and BHV-1 causes more severe disease in calves than either virus by itself, and antibody responses are delayed and lower in calves infected with both viruses (Ghram et al., 1989).
BPIV3 is transmitted by direct contact between animals and by aerosol infection.
Impact: EconomicTop of page
The economic impact of BPIV3 by itself is not known. BPIV3 is one of the factors associated with enzootic pneumonia in housed dairy calves, veal calves and beef calves in crowded calving grounds, and bovine respiratory disease (BRD, shipping fever) in feedlot cattle. BRD has been reported to cause 31% of cattle deaths in the USA and enzootic pneumonia can be responsible for up to 30% of all dead calves in dairy herds is and the single largest cause of death in veal calf farms (van Donkersgoed et al., 1993; Vogel and Parrott, 1994; Radostits et al., 2000b). The economic losses for the beef industry in the USA due to death, treatment, decreased animal performance, and labour have been estimated at US $624 million per year (Anon., 1992). Morbidity rates for enzootic pneumonia in dairy cattle and BRD in beef cattle are 80-100% (van Donkersgoed et al., 1993; Vogel and Parrott, 1994; Radostits et al., 2000a,b).
One report by Senf et al. (1988) indicates the economic impact of BPIV3 infection. BPIV3 was isolated from 202 lung samples of calves with a respiratory disease complex over a 5-year period on 131 premises, and immunization with a BPIV3 vaccine reduced economic losses and disease.
Zoonoses and Food SafetyTop of page
BPIV3 is closely related to human PIV3 and can infect humans. However, a relatively high dose of BPIV3 is required for the infection of humans (Collins et al., 1996). Therefore, infection by consumption of BPIV3-contaminated meat from cattle, (particularly from the respiratory organs) is unlikely. BPIV3 does not survive in properly cooked meat. In addition, a live BPIV3 candidate vaccine for humans has been tested and was found to be safe and induce immunity in children (Karron et al., 1995; Collins et al., 1996). Nevertheless, a period of 3-4 weeks disease-free before slaughter of cattle is recommended for livestock previously infected with BPIV3.
Disease TreatmentTop of page
Treatment of BPIV3- infected calves with alpha-interferon has been reported (Kishko and Mukvich, 1998).
Treatment must take into consideration the frequent secondary bacterial pneumonia following a BPIV3 infection. Sick animals should be isolated from healthy ones and, in consultation with a veterinarian, treated with antibiotics to prevent secondary infections.
Prevention and ControlTop of page
Disease prevention and control is based on good husbandry, management strategies to decrease stress, and appropriate vaccination (Ballásh and Kudron, 1993; Elze and Selbitz, 1993; Rebhun et al., 1995; Radostits et al., 2000a,b). Many guidelines that address these factors are available for local situations from government institutions.
With respect to enzootic pneumonia, the animal population at risk for development of pneumonia are housed dairy and veal calves and to a lesser extent beef calves of 2 weeks and older (Radostits et al., 2000b).
Steps to prevent and control pneumonia include the following:
- Make sure that calves drink adequate colostrum containing a high level of antibodies to BPIV3 (and other respiratory disease-causing infectious agents; Hofmann et al., 1991; Barringer and Rosenberg, 1995).
- Ensure that calves are fed and housed well.
- Group and house calves by size and age, and avoid overcrowding.
- Isolate newly purchased calves for a few weeks.
- Follow an all-in, all-out procedure; clean and disinfect pens, and leave pens empty for a few days between groups.
- Keep sick calves separated from healthy ones, and treat them with antibiotics in consultation with a veterinarian.
- Obtain a diagnosis of the causative agent.
- Keep health records on calves.
- Vaccinate calves against respiratory diseases with a vaccine including BPIV3 when passive antibodies have decreased, which usually occurs at 4 months and give a booster at 6 months, followed by yearly booster immunizations (Rebhun et al., 1995).
Many effective BPIV3 vaccines are available; modified-live vaccines for intra-nasal and intra-muscular administration and killed products for intra-muscular use (van Donkersgoed et al., 1991; Fulton et al., 1995; Hermülheim and Wittkowski, 1995). Intra-nasal BPIV3-containing products elicit a fast local immune response.
Bovine Respiratory Disease
With respect to BRD (shipping fever) in feedlot cattle, the animals at risk for development of pneumonia are beef calves during the first weeks after arrival (Martin and Bohac, 1986; Martin et al., 1989; Radostits et al., 2000a). The cause of disease is multifactorial and greatly affected by management practices and degree of stress. Generally calves arriving in feedlots seroconvert to several respiratory viruses including BPIV3 within the first month (Fulton et al., 2000; Radostits et al., 2000a).
Risk factors associated with disease include increased mixing of calves from different origins, month of purchase, duration of transport, and weather conditions at arrival (Radostits et al., 2000a). To reduce stress and disease associated with transport and entering into a feedlot, a program of preconditioning and preimmunization is undertaken in which calves are dehorned, castrated and vaccinated before weaning by the cow-calf producer. Immunization of the calves with a vaccine containing BPIV3 is recommended during preconditioning and at arrival at the feedlot. Many modified-live and killed BPIV3 vaccines are available usually combined with other viral and bacterial products. Sick animals should be isolated from healthy calves and treated with appropriate antibiotics to prevent bacterial disease, in consultation with a veterinarian.
The efficacy of the current vaccines, irrespective of the formulation, is fair in dairy cattle, but with the different management issues confronting the feedlot industry, the control of UF/BRDC is complicated using the vaccination approach (Elankumaran, 2013). There are conflicting reports on the efficacy of the intranasal vaccine formulations in comparison with parenteral live attenuated vaccines (Ellis, 2010). Both types of vaccine are capable of inducing local and systemic protective antibody responses, but the duration and magnitude of response may depend on the status of local and systemic antibody levels at the time of vaccination. Maternal antibodies inhibit the development of active immunity against BPIV3 (Marshall and Frank, 1975; Adair et al., 2000; Fulton et al., 2004).
Contradictory data have been described with respect to the benefit of the use of alpha-interferon for prevention or reduction of disease caused by BPIV3 (Bryson et al., 1989; Kishko and Mukvich, 1998).
ReferencesTop of page
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