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bovine parainfluenza 3 infection

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Datasheet

bovine parainfluenza 3 infection

Summary

  • Last modified
  • 03 January 2018
  • Datasheet Type(s)
  • Animal Disease
  • Preferred Scientific Name
  • bovine parainfluenza 3 infection
  • Overview
  • Bovine parainfluenza virus 3 (BPIV3) is an important pathogen that causes acute upper and lower respiratory tract infections in calves (

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    Compendia
    CAB International
    Wallingford
    Oxfordshire
    OX10 8DE
    UK
    compend@cabi.org
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Pictures

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PictureTitleCaptionCopyright
Calf with enzootic pneumonia.
TitleSymptoms
CaptionCalf with enzootic pneumonia.
Copyright©Paul R. Greenough
Calf with enzootic pneumonia.
SymptomsCalf with enzootic pneumonia.©Paul R. Greenough
Bovine fetal lung cells infected with BPIV3. Cells were fixed 72 hours post-infection and stained with hematoxylin/eosin. Note the multinuclear cell (synctium) at the centre of the picture.
TitleInfected lung cells
CaptionBovine fetal lung cells infected with BPIV3. Cells were fixed 72 hours post-infection and stained with hematoxylin/eosin. Note the multinuclear cell (synctium) at the centre of the picture.
CopyrightS. van Drusen Littel-van den Hurk
Bovine fetal lung cells infected with BPIV3. Cells were fixed 72 hours post-infection and stained with hematoxylin/eosin. Note the multinuclear cell (synctium) at the centre of the picture.
Infected lung cellsBovine fetal lung cells infected with BPIV3. Cells were fixed 72 hours post-infection and stained with hematoxylin/eosin. Note the multinuclear cell (synctium) at the centre of the picture.S. van Drusen Littel-van den Hurk
Detection of BPIV3 antigen by indirect immunofluorescence. Bovine fetal lung cells were fixed 72 hours post-infection and stained with anti-fusion protein monoclonal antibody and anti-species lgG linked to fluoresceine. Note the fluorescence in the cytoplasm of infected cells.
TitleBPIV3 antigen
CaptionDetection of BPIV3 antigen by indirect immunofluorescence. Bovine fetal lung cells were fixed 72 hours post-infection and stained with anti-fusion protein monoclonal antibody and anti-species lgG linked to fluoresceine. Note the fluorescence in the cytoplasm of infected cells.
CopyrightS. van Drusen Littel-van den Hurk
Detection of BPIV3 antigen by indirect immunofluorescence. Bovine fetal lung cells were fixed 72 hours post-infection and stained with anti-fusion protein monoclonal antibody and anti-species lgG linked to fluoresceine. Note the fluorescence in the cytoplasm of infected cells.
BPIV3 antigenDetection of BPIV3 antigen by indirect immunofluorescence. Bovine fetal lung cells were fixed 72 hours post-infection and stained with anti-fusion protein monoclonal antibody and anti-species lgG linked to fluoresceine. Note the fluorescence in the cytoplasm of infected cells.S. van Drusen Littel-van den Hurk
Immunohistological staining of lung tissue of a calf infected with BPIV3. Tissue sections were fixed and stained with rabbit antibodies to BPIV3 and avidin-biotin immunoperoxidase complex using diamonobezidine, and counterstained with hematoxylin. Note presence of BPIV3 antigen (red colour) in broncheolar epithelium.
TitleInfected BPIV3 lung tissue
CaptionImmunohistological staining of lung tissue of a calf infected with BPIV3. Tissue sections were fixed and stained with rabbit antibodies to BPIV3 and avidin-biotin immunoperoxidase complex using diamonobezidine, and counterstained with hematoxylin. Note presence of BPIV3 antigen (red colour) in broncheolar epithelium.
CopyrightD. Haines/WCVM, Saskatoon, Canada.
Immunohistological staining of lung tissue of a calf infected with BPIV3. Tissue sections were fixed and stained with rabbit antibodies to BPIV3 and avidin-biotin immunoperoxidase complex using diamonobezidine, and counterstained with hematoxylin. Note presence of BPIV3 antigen (red colour) in broncheolar epithelium.
Infected BPIV3 lung tissueImmunohistological staining of lung tissue of a calf infected with BPIV3. Tissue sections were fixed and stained with rabbit antibodies to BPIV3 and avidin-biotin immunoperoxidase complex using diamonobezidine, and counterstained with hematoxylin. Note presence of BPIV3 antigen (red colour) in broncheolar epithelium.D. Haines/WCVM, Saskatoon, Canada.
Bovine lung with fibrinous pneumonia caused by Pasteurella haemolytica and bovine parainfluenzavirus 3, affecting the cranial lobe, the middle lobe and the cranio-ventral portions of the caudal lobes of the lungs.
TitlePathology - fibrinous pneumonia
CaptionBovine lung with fibrinous pneumonia caused by Pasteurella haemolytica and bovine parainfluenzavirus 3, affecting the cranial lobe, the middle lobe and the cranio-ventral portions of the caudal lobes of the lungs.
Copyright©Paul R. Greenough
Bovine lung with fibrinous pneumonia caused by Pasteurella haemolytica and bovine parainfluenzavirus 3, affecting the cranial lobe, the middle lobe and the cranio-ventral portions of the caudal lobes of the lungs.
Pathology - fibrinous pneumoniaBovine lung with fibrinous pneumonia caused by Pasteurella haemolytica and bovine parainfluenzavirus 3, affecting the cranial lobe, the middle lobe and the cranio-ventral portions of the caudal lobes of the lungs.©Paul R. Greenough

Identity

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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

Overview

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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 Affected

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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.

Distribution

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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 Table

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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/RegionDistributionLast ReportedOriginFirst ReportedInvasiveReferenceNotes

Asia

ChinaWidespreadZhu et al., 2011; Wen et al., 2012; Wang et al., 2014
IndiaLocalisedSingh, 1991
IndonesiaWidespreadItoh et al., 1989
IranPresentEzzi et al., 2013; Farzinpour et al., 2014
JapanWidespreadKomoda et al., 1988; Kadoi et al., 1998
Korea, Republic ofWidespreadKim et al., 1988
Russian Federation
-Russia (Asia)WidespreadZhumabaev and Belousova, 1992; Masimov, 1994
Saudi ArabiaPresentMahmoud and Allam, 2013
SyriaWidespreadTabbaa, 1989; Giangaspero et al., 1992
TaiwanWidespreadLiao et al., 1992
ThailandWidespreadVirakul et al., 1997
TurkeyWidespreadOztürk and Yavru, 1988; Oztürk and Duman, 1992; Ozdarendeli et al., 1997

Africa

Congo Democratic RepublicWidespreadJetteur et al., 1988
EgyptWidespreadWassel et al., 1996
MaliWidespreadMaiga and Sarr, 1992
NigeriaWidespreadIbu et al., 1996
South AfricaWidespreadOdendaal et al., 1997
TunisiaWidespreadGhram and Minocha, 1990

North America

CanadaWidespreadEttinger and Feldman, 2000
-AlbertaWidespreadDurham and Hassard, 1990
-OntarioWidespreadMartin and Bohac, 1986; Martin et al., 1989
-SaskatchewanWidespreadDurham and Hassard, 1990; Donkersgoed et al., 1993
MexicoWidespreadMelgarejo et al., 1991
USAWidespreadAnon., 1992; Fulton et al., 2000

South America

ArgentinaWidespreadRuiz et al., 1989; Fulton et al., 2000; Maidana et al., 2012
BrazilWidespreadDal et al., 1989
ChileWidespreadRiedemann et al., 1996
ColombiaPresentBetancur et al., 2010
PeruPresentSolís et al., 2010

Europe

AlbaniaWidespreadIkonomi et al., 1988
AustriaWidespreadCoulibaly, 1990
BelarusLocalisedMuzychin and Letetskii, 1988
BelgiumPresentPardon et al., 2011
BulgariaLocalisedKosarov et al., 1998
CroatiaLocalisedLedinek and Silak, 1995
Czech RepublicLocalisedTrávnícek, 1999
DenmarkWidespreadTegtmeier et al., 1999
FranceWidespreadPenn and Savey, 1990
GermanyWidespreadSenf et al., 1988
GreeceWidespreadKakamoukas et al., 1989
HungaryWidespreadRusvai and Fodor, 1998; Miklós et al., 1999
IrelandWidespreadHealy et al., 1993
ItalyWidespreadMaglione and Rosati, 1988; Moriconi and Gnaccarini, 1991
LithuaniaPresentKestaitiene et al., 2009
NetherlandsWidespreadVerhoeff and Nieuwstadt, 1984
NorwayPresentGulliksen et al., 2009
PolandWidespreadKlimentowski et al., 1995
RomaniaWidespreadCambir and Coman, 1991
Russian FederationPresentPresent based on regional distribution.
-Russia (Europe)WidespreadZhumabaev and Belousova, 1992; Masimov, 1994
-Southern RussiaWidespreadZhumabaev and Belousova, 1992
SlovakiaWidespreadKovác et al., 1995
SpainWidespreadCatalán et al., 1994
SwitzerlandWidespreadLäuchli et al., 1990
UKWidespreadStott et al., 1980
UkraineWidespreadStetsenko et al., 1992
Yugoslavia (former)LocalisedVinkovic and Cac, 1990
Yugoslavia (Serbia and Montenegro)LocalisedLazic et al., 1995

Oceania

AustraliaWidespreadDunn et al., 1998
New ZealandWidespreadMotha et al., 1997; Motha and Hansen, 1998

Pathology

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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).

Diagnosis

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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/Signs

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SignLife StagesType
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 Course

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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).

Although it has been reported that BPIV3 may infect foetuses and cause abortions in cattle, it is not considered a common cause of abortion (Dunne et al., 1973; Swift and Trueblood, 1974).

Epidemiology

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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: Economic

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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 Safety

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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 Treatment

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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 Control

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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.


Enzootic Pneumonia


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).

References

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Adair BM; Bradford HEL; Bryson DG; Foster JC; McNulty MS, 2000. Effect of parainfluenza-3 virus challenge on cell-mediated immune function in parainfluenza-3 vaccinated and non-vaccinated calves. Research in Veterinary Science, 68(2):197-199.

Aguirre AA; Hansen DE; Starkey EE; McLean RG, 1995. Serologic survey of wild cervids for potential disease agents in selected national parks in the United States. Preventive Veterinary Medicine, 21(4):313-322; 51 ref.

Allan EM; Pirie HM; Selman IE; Snodgrass DR, 1978. Some characteristics of a natural infection by parainfluenza-3 virus in a group of calves. Veterinary Science, 24:339-346.

Andrewes C; Pereira HG; Wildy P (eds), 1978. Viruses of vertebrates: Paramixoviridae. London, UK: Cassell & Co Ltd, 221-254.

Anon., 1992. Cattle and calves death loss. National Agricultural Statistics Services, USDA.

Assaf R; Montpetit C; Marsolais G, 1983. Serology of bovine parainfluenza virus type 3: comparison of the enzyme-linked immunosorbent assay and hemagglutination. Canadian Journal Comparative Medicine, 47:140-142.

Ballásh A; Kudron E, 1993. Observations on the PI-3 virus infection of calves kept in pens and later in sheds. Magyar állatorvosok Lapja, 48(5):281-285; 13 ref.

Barringer LS; Rosenberg JB, 1995. Better colostrum. Large Animal Veterinarian, 50(6):22-23; 2 ref.

Basaraba RJ; Brown PR; Laegreid WW; Silflow RM; Evermann JF; Leid RW, 1993. Suppression of lymphocyte proliferation by parainfluenza virus type 3-infected bovine alveolar macrophages. Immunology, 79(2):179-188; 40 ref.

Bechmann G, 1997. Serological diagnosis of cattle viruses in sheep. Deutsche Tierärztliche Wochenschrift, 104(8):321-324; 4 ref.

Betancur Hurtado C; Orrego Uribe A; González Tous M, 2010. Seroepidemiological study of parainfluenza 3 virus in bovines with reproductive failure, from Monteria-Colombia. (Estudio seroepidemiológico del virus de parainfluenza 3 en bovinos del municipio de Montería (Colombia) con trastornos reproductivos.) Revista de Medicina Veterinaria, No.20:63-70. http://publicaciones.lasalle.edu.co/images/openacces/Revistas/veterinaria/MV20/estudio_seroepidemiologico.pdf

Betts AO; Jennings AR; Omar AR; Page ZE; Spence JB; Walker RG, 1964. Pneumonia in calves by parainfluenza virus type 3. Veterinary Record, 76:382-384.

Breker-Klassen MM; Yoo DongWan; Babiuk LA, 1996. Comparisons of the F and HN gene sequences of different strains of bovine parainfluenza virus type 3: relationship to phenotype and pathogenicity. Canadian Journal of Veterinary Research, 60(3):228-236; 64 ref.

Brown TT; Ananaba G, 1988. Effect of respiratory infections caused by bovine herpesvirus-1 or parainfluenza-3 virus on bovine alveolar macrophage functions. American Journal Veterinary Research, 49:1447-1451.

Bryson DG; McFerran JB; Ball HJ; Neil SD, 1978. Observations on outbreaks of respiratory disease in housed calves. II. Pathological and microbiological findings. Veterinary Record, 103:503-509.

Bryson DG; McFerran JB; Ball HJ; Neil SD, 1979a. Observations on outbreaks of respiratory disease in caves associated with parainfluenza type 3 virus and respiratory syncytial virus infection. Veterinary Record, 104:45-49.

Bryson DG; McNulty MS; Ball HJ; Neil SD; Connor TJ; Cush PF, 1979b. The experimental production of pneumonia in calves by intranasal inoculation of parainfluenza type 3 virus. Veterinary Record, 105:566-573.

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