Respirator y Disease

of the Bovine Neonate

Keith P. Poulsen, DVMa,b,*, Sheila M. McGuirk, DVM, PhDa

KEYWORDS
 Bovine  Calf  Neonate  Hypoxia
 Persistent pulmonary hypertension  Pneumonia
 Pneumothorax

Respiratory disease is a constant challenge for dairy replacement heifer rearing sys-
tems, and is responsible for 21.3% of mortality in preweaned calves and 50.4% of
deaths in weaned heifers.1 There are many negative long-term consequences for
survivors of subclinical, clinical, and chronic calf pneumonia including poor growth, re-
productive performance, milk production, and longevity.2–4 These calves also become
sources of infection for other calves, and can cause outbreaks after weaning in group
pens.5 Contamination of the environment with bacterial and viral pathogens is the ob-
vious source of respiratory disease in calves. When reviewing the literature and exam-
ining cases seen both in the authors’ hospital and during herd investigations, however,
it was realized that treatment and prevention of calf pneumonia has evolved beyond
recommendations for antibiotic therapy and vaccination protocols. The high cost of
replacement heifers and the development of reproductive technologies have in-
creased the need to detect and treat high-risk neonates suffering from respiratory dis-
ease. Many times those calves serve as sentinels for infectious disease that direct calf
management decisions on the farm. This article discusses the normal physiologic
changes from the uterine environment through parturition and methods to monitor
the high-risk or abnormal neonate. Covered are causes of respiratory disease and dif-
ferent strategies for diagnosis and treatment that can be applied to herd investigations
or individual animals. All herd investigation tools and forms can be found at the follow-
ing Web site: http://www.vetmed.wisc.edu/dms/fapm/fapmtools/calves.htm.

THE POSTNATAL PERIOD, HYPOXIA, AND HYPERCAPNIA

Many physiologic changes occur rapidly in the transition from fetal life to the neonatal
period. At parturition the neonate needs to assume responsibility for oxygenating its

a
Department of Medical Sciences, University of Wisconsin-Madison School of Veterinary
Medicine, 2015 Linden Drive, Madison, WI 53706, USA
b
Department of Pathobiological Sciences, University of Wisconsin-Madison School of Veteri-
nary Medicine, Madison, WI 53706, USA
* Corresponding author. Department of Medical Sciences, University of Wisconsin-Madison
School of Veterinary Medicine, 2015 Linden Drive, Madison, WI 53706.
E-mail address: [email protected] (K.P. Poulsen).

Vet Clin Food Anim 25 (2009) 121–137

doi:10.1016/j.cvfa.2008.10.007 vetfood.theclinics.com
0749-0720/08/$ – see front matter ª 2009 Elsevier Inc. All rights reserved.
122 Poulsen & McGuirk

own blood from atmospheric air, and maintaining a normal blood pH and body tem-
perature.6 In utero, the numerous placentomes that are distributed on the endometrial
surface provide oxygen and nutrient-rich blood to the fetal placenta. Distribution of the
oxygen and nutrients is accomplished by the fetal circulation shunting blood away
from the pulmonary circulation by way of the ductus arteriosus and foramen ovale,
which is facilitated by hypoxia-induced pulmonary arterial constriction.7 The fetus is
quite hypoxic (80% O2 saturation, PaO2 of 38 mm Hg) relative to the dam (98%–
100% O2 saturation, PaO2 of 100 mm Hg), but adapts well to this environment because
of efficient O2 extraction from maternal placental blood with fetal hemoglobin’s high
affinity for O27–9 and by increasing blood flow from nonessential organs to the brain,
heart, and adrenal glands.10
At birth massive changes in lung function and arterial blood gases occur as the fetal
lung fluid is removed with uterine contractions and absorbed by the pulmonary circu-
lation and lymphatics as the calf begins to breathe.11 Before stage 2 labor, the fetus
should not be hypoxic as long as the umbilical cord remains attached,8 but during fetal
expulsion, rupture of the fetal membranes and separation of the umbilical vessels lead
to hypoxia and respiratory and metabolic acidosis.12,13 Respiratory acidosis (hyper-
capnia), detected by the chemosensitive area in the medulla, is the most important
stimulus for respiration. This is aided by tactile stimulation from the dam (ie, licking)
and a decrease in environmental temperature relative to in utero conditions.14,15 Hyp-
oxia, detected by peripheral chemoreceptors in the carotid and aortic bodies, does
not have a significant direct effect on the respiratory center in the brain.14 Dystocia
can result in a severe respiratory and metabolic acidosis that may require treatment
or can result in long-term detrimental effects on the neonate, such as hypoxic-ische-
mic encephalopathy.16 The degree of respiratory acidosis is dependent on the time
between loss of maternal blood supply to the fetus and successful respiration.8 Met-
abolic acidosis is caused by lactic acid accumulation during hypoxia.17,18 Healthy
calves have a surprising ability, however, to self-correct hypercapnia and hypoxia
within the first hours of life.19–21 As respiration continues to increase pulmonary blood
flow and improve oxygenation, the foramen ovale and ductus arteriosus close to end
fetal circulation.8
Several methods have been described to monitor acid-base status and pulmonary
function, and predict morbidity and mortality caused by respiratory disease in the ne-
onate. Sternal recumbency should be attained within 2 to 3 minutes and the normal
calf should attempt to stand within 15 to 30 minutes after birth. Hypoxic neonates,
likely to be affected by respiratory acidosis, have a weak to absent suckle reflex,
have difficulty maintaining sternal recumbency, and require more time to stand.22
The Apgar scoring index can be used to assess neonatal viability and predict early
signs of peripartum asphyxia.23 Perhaps more practical on the dairy, Schuijt and
Taverne24 described the time to attain sternal recumbency as a measure of neonatal
viability. They reported a negative correlation between neonatal vitality and increased
time for the calf to achieve sternal recumbency after birth. Calves that took greater
than 15 minutes to achieve sternal recumbency had an 84% predictive value for non-
vitality. Other critical elements of the physical examination when assessing for the
presence of respiratory disease include mucous membrane color (vulvar mucous
membranes); character and frequency of the respiratory effort; and thoracic
auscultation.
If available, pulse oximetry and blood gas analysis can be valuable to assess pulmo-
nary function and acid-base status. Pulse oximetry was validated in the calf as a rela-
tively accurate, noninvasive, immediate, and portable method to monitor oxygen
saturation (SaO2).25 Bleul and Kähl26 describe using pulse oximetry during stage 2
 Respiratory Disease of the Bovine Neonate 123

labor to assess pulmonary function in valuable calves during delivery, because fetal re-
flexes are poorly correlated with fetal vitality in cattle.27 Despite the challenge of using
the oximeter during parturition, calves with low SaO2 (<30%) for at least 2 minutes in
stage 2 labor had a high predictive value for acidosis (blood pH <7.2).26 In a hospital set-
ting, blood gas analysis is a direct measure of PO2, PCO2, concentration of bicarbonate
(HCO3-), base excess, SaO2, and pH. Reference values for acidotic calves (pH <7.2) and
normal calves (pH R7.2) were recently reported (Table 1).28 Evaluating pH and base ex-
cess values from venous blood are established methods;12–15,29 however PO2 and PCO2
need to be measured from arterial blood because of the CO2 and O2 exchange in pe-
ripheral tissues.30,31 There is no significant difference between using arterial blood
from peripheral versus central arteries32 and the brachial, lateral metatarsal, or the
branches of the caudal auricular artery are suitable collection sites.28,33 Plastic has re-
placed glass syringes in many settings because of cost, convenience, and resistance to
breakage. It is important to note, however, that blood in plastic syringes needs to be an-
alyzed immediately to ensure accuracy of the PO2 measurement.34,35
Treatment of hypoxia and hypercapnia can be a challenge. Calves with significant
hypoxia can be started on humidified oxygen by nasal administration at a rate of 2
to 10 L/min. Hypercapnia may persist despite oxygen therapy. The ventilatory drive
caused by hypercapnia and associated respiratory acidosis is significantly stronger
than the drive caused by hypoxemia. These calves might require treatment with respi-
ratory stimulants, such as the methylxanthines (caffeine and aminophylline) or
doxapram hydrochloride. Both of these drugs decrease the need for mechanical ven-
tilation.36 Methylxanthines directly stimulate the respiratory center, improve diaphrag-
matic contractility, and antagonize adenosine, which slows respiration.36,37 Caffeine
(NoDoz, 200 mg/tab) is readily available as an over-the-counter product but its oral
bioavailability has been recently questioned in foals.38 Extrapolated from equine
doses, caffeine can be administered orally or per rectum with a 10 mg/kg loading
dose followed by a 2.5 to 3 mg/kg every 24 hour maintenance dose.39 When using am-
inophylline in the authors’ hospital the doses reported for horses are used (4–10 mg/kg
every 8–12 hours)40 as a constant rate infusion (10–30 mg/kg/d). Doxapram hydro-
chloride stimulates the medullary respiratory centers by way of the aortic and carotid
body chemoreceptors and can be given at a dose of 0.5 mg/kg IV or 5 to 10 mg/kg
injected at the base of the tongue for emergency resuscitation and anoxia.40–42 Dox-
apram has a history of poor availability to practitioners and has been reported to in-
crease cerebral oxygen consumption and decrease cerebral blood flow, which has
negative long-term consequences for the neonate.43 A study in foals using an exper-
imentally induced hypercapnia model, however, reported that doxapram restored
ventilation without neurologic side effects in a dose-dependent manner.38 Acupres-
sure is an alternative therapy for anoxia that has occasionally been used in small
and large animal neonatology. In calves, the authors use a 20-gauge, 1-in hypodermic
needle placed in the nasal planum immediately after parturition if the calf is anoxic. The
mechanism behind this technique is stimulation of the Renzhong acupoint, which in-
creases phrenic nerve activity.44 Ideally, serial blood gas analysis should be done to
monitor the calf’s response to whichever therapies are implemented. Calves with per-
sistent hypercapnia despite therapeutic intervention are candidates for mechanical
ventilation if available.

PERSISTENT PULMONARY HYPERTENSION

Persistent pulmonary hypertension is a syndrome characterized by significant cellular

proliferation and extracellular matrix protein production in pulmonary endothelial cells.
 124
Poulsen & McGuirk
Table 1
Mean (SD) values of arterial and venous blood gas and acid-base analyses in 57 newborn calves from birth to 24 hours

Time of Sampling
Variable Blood At Birth 30 Minutes 4 hours 12 Hours 24 Hours Pa Pb
pH Arterial 7.30 (0.06) 7.36 (0.04) 7.38 (0.03) 7.42 (0.03) 7.43 (0.04) <0.001 >0.05
Venous 7.24 (0.09) 7.30 (0.04) 7.33 (0.03) 7.38 (0.04) 7.40 (0.06) <0.001
PCO2 (mm Hg) Arterial 57.31 (4.98) 52.58 (5.00) 48.70 (3.73) 43.71 (4.75) 44.22 (4.32) <0.001 <0.001
Venous 67.34 (10.39) 58.23 (6.45) 54.38 (6.10) 47.03 (5.75) 46.67 (6.24) <0.001
PO2 (mm Hg) Arterial 45.31 (16.02) 58.08 (13.12) 67.66 (14.55) 71.89 (8.32) 66.77 (14.21) <0.001 <0.05
Venous 20.94 (5.30) 27.95 (5.42) 29.15 (4.41) 29.33 (5.52) 27.62 (3.04) <0.001
HCO-3 (mmol/l) Arterial 26.76 (3.39) 28.01 (2.44) 27.40 (2.32) 26.96 (2.94) 28.31 (3.26) >0.05 >0.05
Venous 27.24 (3.70) 27.48 (3.81) 27.42 (3.18) 26.42 (2.82) 27.87 (3.35) >0.05
Base excess (mmol/L) Arterial 0.86 (4.12) 2.9 (2.88) 2.52 (2.64) 2.78 (3.23) 4.42 (3.59) >0.05 >0.05
Venous 1.01 (3.49) 1.53 (4.37) 1.89 (3.48) 1.59 (3.08) 3.40 (3.92) >0.05
SO2 (%) Arterial 64.16 (20.82) 82.08 (9.98) 89.23 (6.84) 92.84 (2.32) 89.75 (8.31) <0.001 >0.05
Venous 22.64 (10.00) 39.26 (10.98) 44.19 (9.39) 47.41 (12.06) 47.81 (15.41) <0.001

Abbreviations: HCO-3, bicarbonate; PCO2, partial pressure of carbon dioxide; PO2, partial pressure of oxygen; SO2, oxygen saturation.
a
Analysis of variance for repeated measures within groups.
b
Analysis of variance for repeated measures between groups.
Data from Bleul U, Lejeune B, Schwantag S, et al. Blood gas and acid-base analysis of arterial blood in 57 newborn calves. Vet Record 2007;161:688–91.
 Respiratory Disease of the Bovine Neonate 125

It occurs in response to persistent hypoxemia and vasoconstriction, which causes re-

version to fetal pulmonary circulatory patterns with right-to-left shunting. Pulmonary
hypertension can also be secondary to failure of the neonate’s cardiopulmonary circu-
lation to transition from the fetal state.45–48 The disorder has been recognized in
human and equine neonates, and the calf is used as a model to study pulmonary
hypertension.49–53 Pulmonary hypertension can be secondary to many different
factors, such as persistent hypoxia caused by pneumonia, high altitude, or meconium
aspiration, but the primary disorder is often idiopathic. Recently, persistent pulmonary
hypertension has been increasingly recognized in calves derived from somatic cell
clone technology.54–58
Calves with persistent pulmonary hypertension are hypoxic (PaO2 <80 mm Hg) and
tend to be hypercapnic. Diagnosis can be based on repeated arterial blood gas mea-
surements when all other causes of hypoxemia are ruled out.59 Other diagnostic tests
for persistent pulmonary hypertension include radiographs or CT, cardiac catheteriza-
tion, and echocardiography. Radiographs and CT show atelectasis and diminished
vascular patterns from pulmonary hypoperfusion. Cardiac catheterization shows
elevated pressure in the pulmonary artery, right ventricle, and right atrium.60,61
Treatment of persistent pulmonary hypertension centers on oxygen supplementa-
tion and mechanical ventilation if hypoxemia and hypercapnia persist. If acidosis is
severe, bicarbonate therapy may be indicated. Nitric oxide is frequently used in human
and equine neonates as a vasodilator.62,63 Vasodilation with a phosphodiesterase-5
inhibitor, sildenafil (Viagra) given orally or as a suppository, has been used to treat per-
sistent pulmonary hypertension in human infants64,65 and foals61 with varying success.

ASPIRATION PNEUMONIA

Aspiration pneumonia occurs when solid materials, typically a liquid or meconium, are
inhaled. The most common cause of neonatal aspiration pneumonia seen in the au-
thors’ practice is from misuse of oral esophageal feeders. The use of oral esophageal
feeders to ‘‘tube-feed’’ a calf has increased on farms to ensure timely feeding of an
appropriate volume of clean, good-quality colostrum. Feeding calves with bottles
can be time consuming and calves left to suckle the dam have high rates of failure
of passive transfer.66 Even though the esophageal groove does not close when using
esophageal feeders, there is no significant difference in calf serum IgG concentrations
or morbidity when compared with calves that suckle colostrum from a bottle.67 Proper
training of on-farm personnel is important to ensure placement of the feeder in the
esophagus. Important points to review with personnel responsible for calf feeding
are to use lubrication, to use an oral esophageal feeder that has a mechanism to con-
trol flow rates in case problems occur, and to maintain the calf’s neutral head position
during feeding while the calf is standing or in sternal recumbency.
Another cause of aspiration pneumonia, meconium aspiration, is associated with fe-
tal distress syndrome and frequently results in increased mortality.68 Gross and histo-
pathologic lesions are similar to those described in human infants with meconium
aspiration syndrome and consist of acute and long-term sequelae.68 In the acute
phase of the syndrome, complete and partial airway obstruction leads to hyperinflated
pulmonary tissue, ventilation-perfusion mismatch, pulmonary hypertension, and in-
creased risk for pneumothorax.69–71 Chronic effects of meconium aspiration include
chemical pneumonitis and disruption of surfactant function, which has been proposed
to be a significant contributor to meconium aspiration syndrome.72–82
With large quantities of aspirated foreign material the calf may die acutely. Gener-
ally, the aspiration causes a gangrenous bronchopneumonia and animals display
126 Poulsen & McGuirk

the typical clinical signs of depression, respiratory distress, fever, and malodorous
breath. Auscultation of the lung fields bilaterally may reveal crackles, wheezes, and
pleural friction rubs.83 The calf may be hypoxic and hypercapnic on arterial blood
gas analysis. History and clinical signs aid in diagnosis; however, hematology, radio-
graphs, and pleural ultrasound examination are required to define better the extent of
disease. Treatment almost always involves long-term antimicrobial and anti-inflamma-
tory therapy.

BACTERIAL PNEUMONIA

Bacterial pneumonia in the first few days of life can be from sepsis, aspiration pneu-
monia, or gross bacterial contamination of colostrum. Most septic calves with pulmo-
nary disease present depressed and lethargic. The physical examination, specifically
thoracic auscultation, is not always consistent with pulmonary disease. The authors
have found that inducing a cough by firmly shaking the trachea at the level of the larynx
is helpful in confirming the diagnosis of pulmonary disease. Definitive diagnosis re-
quires radiographs, transtracheal wash, or bronchial alveolar lavage. The authors
have implemented bronchial alveolar lavage in the clinic and on-farm as an efficient
way to get diagnostic samples representative of lower airway fluid for culture (Sheila
M. McGuirk, DVM, PhD, unpublished data, 2007).
The bronchial alveolar lavage procedure is described next. Calves are sedated with
xylazine (0.1 mg/kg IM) and the head is restrained by pushing the poll down while el-
evating the nose to ease placement of a flexible 10-  36-in French catheter with
a 3-mL balloon cuff (Mila International, Medical Instrumentation for Animals, Florence,
Kentucky) into the trachea by way of the nares (Fig. 1). Repeated coughing is ob-
served with proper placement of the catheter. The catheter is passed until it is wedged
in a terminal bronchus and the balloon is inflated to create a seal to allow alveolar

Fig. 1. This is an example of an on-farm bronchial alveolar lavage procedure. A flexible 10F
catheter has been inserted into the trachea by the nares and advanced until it is wedged in
a terminal bronchus. See text for further details on the procedure.
 Respiratory Disease of the Bovine Neonate 127

lavage. A total of 240 mL of 0.9% NaCl is lavaged (two separate 120-mL samples). Fol-
lowing administration, as much saline as possible is then aspirated back through the
catheter. An appropriate sample volume is 10 to 40 mL of clear to mildly turbid, foamy
fluid. The samples from both lavages are mixed and should be refrigerated or analyzed
fresh within 2 hours. Five milliliters of sample should be submitted for aerobic and
Mycoplasma cultures. The remaining fluid should be submitted for cytologic interpre-
tation from cytospin and direct smear. Bronchial alveolar lavage fluid that yields ho-
mogenous (>106 CFU/mL) bacterial or positive Mycoplasma bovis culture is
considered abnormal. A disproportionate decrease in the percentage of macrophages
(<75%) or an elevation in neutrophils (>25%) provides evidence of an inflammatory re-
sponse with or without a positive culture. Using this technique it is possible to sample
six to eight calves in a 2-hour period. Identifying which calves are good candidates for
bronchial alveolar lavage during an on-farm herd investigation can be challenging. The
authors have developed a respiratory disease screening tool (Fig. 2) to identify these
calves for diagnostic testing and treatment that can be used by veterinarians and farm
personnel.5,84,85 This tool can be found at http://www.vetmed.wisc.edu/dms/fapm/
fapmtools/calves.htm.
Because the topic of interest is the calf, it is important to note that sepsis and bac-
teremia can cause interstitial pneumonia. Blood culture is important for diagnosis in
these cases and fecal coliforms, most notably Escherichia coli, are the most com-
monly isolated bacteria from bacteremic calves.86,87 Recently, Salmonella dublin
has become increasingly more prevalent in septic calves admitted to the authors’ hos-
pital. S dublin is shed in colostrum and milk, and is associated with severe interstitial
pneumonia along with fever, depression, and gastrointestinal disease.88–90 Antemor-
tem diagnostics submitted in the authors’ hospital when S dublin is suspected include
blood culture, fecal culture, and bronchial alveolar lavage. It is important to send Sal-
monella isolates for speciation. Postmortem samples should also include culture of
liver, lung, and spleen.
Treatment is often initiated at the farm with one or more broad-spectrum antibiotics.
Antibiotic therapy can be tailored to culture and sensitivity results, and in the authors’
opinion should be continued for a minimum of 6 days (Table 2). For herd investiga-
tions, nasal swabs can be used to screen for Mycoplasma sp and to guide antibiotic
therapy. To accomplish this, six untreated calves are sampled with two deep nasal
swabs with flexible culturettes that contain transport media for aerobic and anaerobic
bacteria (BBL Culture Swab Plus, Benton Dickenson, Sparks, Maryland). One swab is
used for bacterial culture and the other is submitted for Mycoplasma sp culture.5 Clin-
ical response to therapy or complete blood cell analysis with fibrinogen can be used in
the decision to extend antibiotic therapy. Depending on severity of clinical signs, sup-
portive care with anti-inflammatory drugs, nutritional support, and nasal administra-
tion of oxygen may be indicated.
Prevention of bacterial sepsis and associated pneumonia centers on providing the
calf with appropriate amounts of maternal antibodies for passive transfer by maternal
colostrum.81 Herds that have problems with gross bacterial contamination of colos-
trum or those that are trying to decrease the prevalence of pathogens present in ma-
ternal colostrum including Mycobacterium paratuberculosis, S dublin, and bovine
leukosis virus should use a colostrum replacement product that provides the calf
with a minimum of 175 g of immunoglobulin.89,91–96 Prompt removal of the calf from
the maternity pen is perhaps equally important in preventing exposure of the animal
to a highly contaminated environment. The early environment poses a high risk for
pathogen exposure to the calf trying to stand and frequently crashing head first into
the maternity pen pack. In addition, calves attempting to nurse frequently suckle other
128 Poulsen & McGuirk

Fig. 2. (A) Calf respiratory scoring chart developed to identify calves for diagnostic treat-
ment and treatment. Calves are assessed based on four categories: rectal temperature, nasal
discharge, cough, and eye or ear. Scores from each category are combined to come up with
a total respiratory score. (B) Calf health scoring criteria for the scoring chart pictured in (A).
 Table 2
Antibiotics commonly used to treat respiratory disease in dairy replacement heifers

Dose for 45-kg Label for

Drug Antibiotic Class Trade Name Dosage (100-lb) Calf Route Frequency Mycoplasma?
Trimethoprim-sulfa Sulfonamides Tribrissen 20 mg/kg, (960 mg tablet) Oral 1. Calves <2 wk: No
40 mg/kg 1 tablet, BID for 6 d
loading dose 2 tablet 2. Calves
loading dose 2–3 wk:
TID for 6 d
Ceftiofur b-lactams Naxcel 2.2 mg/kg 2 mL IM, SQ, or IV SID No
Excenel 2.2 mg/kg 2 mL IM or SQ SID No

Respiratory Disease of the Bovine Neonate

Exceed 6 mg/kg 1.5 mL SQ at the base Once No
of the ear
Florfenicol Florfenicols Nuflor 20 mg/kg 3 mL IM in the neck Q 48 h, 3 doses No
40 mg/kg 6 mL SQ in the neck Once No
Tilmicosin Macrolides Micotil 10 mg/kg 1.5 mL SQ in the neck Q 48 h, 3 doses No
Tulathromycin Macrolides Draxxin 2.5 mg/kg 1.1 mL SQ in the neck Once Yes
Enrofloxacin Fluoroquinolones Baytril 100 7.5–12.5 mg/kg 3.5–5.5 mL SQ Once Noa
2.5–5 mg/kg 1.5–2 mL SQ SID for 6 d Noa
a
Labeled for treatment of bovine respiratory disease in dairy replacement heifers less than 20 months of age. Off-label use of fluoroquinolones is strictly
prohibited. In mixed respiratory infections, Mycoplasma bovis has been shown to be susceptible to enrofloxacin.124,125

129
130 Poulsen & McGuirk

prepartum cows and make erratic nursing attempts on potentially heavily contami-
nated areas (tail, hock, brisket).97–99 These normal behaviors in the maternity pen
put calves at risk of massive oral contamination and possible colonization of the gas-
trointestinal tract. This along with an exposed umbilicus and high concentration of
aerosolized bacteria are potential causes of sepsis.87
The calf’s environment after the maternity pen is another source of bacterial patho-
gens that can cause respiratory disease. Calf raisers continue to build naturally venti-
lated barns to be more efficient and provide a more hospitable environment for labor
despite the long-standing recommendations that individual hutches are the ideal en-
vironment to raise preweaned replacement heifers.100–102 Lago and colleagues84 re-
ported that these naturally ventilated calf barns frequently have poor air quality and
despite ventilation, calf stalls may continue to have high aerosolized bacterial counts.
Their recommendations for calf stalls are that there should be a minimum area of 3 m2
or more per calf, solid panels on two sides to provide a physical barrier between
calves, mesh panels in the front and rear to allow air flow, and deep loose bedding
in colder temperatures. A more thorough review of calf barn design can be found in
a previous edition of this publication.103

VIRAL PNEUMONIA

The most commonly identified causes of viral pneumonia in calves during the first few
weeks of life are bovine herpes virus type 1 or infectious bovine rhinotracheitis and bo-
vine respiratory syncytial virus. Parainfluenza-3 and bovine viral diarrhea virus are also
capable of infecting the respiratory tract and predisposing calves to bacterial pneumo-
nia.104–109 Prevention of viral pneumonia, as with bacterial pneumonia, centers on
passive transfer of maternal antibodies and the innate immune response. As maternal
antibody levels decline, active immunity and vaccination become mainstays of pre-
vention for both viral and bacterial pneumonia. Vaccination recommendations for
calves have been reviewed recently by Chase and colleagues,110 and in the article
by Cortese elsewhere in this issue. Treatment for viral pneumonia is primarily support-
ive and includes metaphylactic or prophylactic antibiotic therapy.

TRAUMATIC INJURY, PNEUMOTHORAX, AND ANAPHYLAXIS

Traumatic injury to the lung has declined over the years because fewer animals have
horns. Fractures are possible in calves if they are stepped on in the maternity pen or
may occur following dystocia.111 Rib fractures are diagnosed during physical exami-
nation and confirmed with radiographs. Treatment is usually not required unless com-
plications, such as myocardial injury, hemothorax, or pneumothorax, occur.112
Pneumothorax of clinical significance is rare in cattle and little information exists in
the literature. Most reports are of adult cattle with rupture of emphysematous bullae
associated with straining, coughing, or parturition.113–116 Pneumothorax has been re-
ported in a preweaned calf as a result of bovine respiratory syncytial virus and in ne-
onates that have undergone mechanical ventilation, both of which may lead to bullae
formation and rupture.117 In a retrospective study of 30 animals, 2 of the cases were
neonates. Traumatic injury was not identified in those cases but blunt thoracic trauma
could not be definitively ruled out.118 The authors suggested idiopathic pneumothorax
secondary to rupture of subpleural blebs or cysts as possible causes.119,120 Meco-
nium aspiration leading to pneumothorax has been reported to be a significant risk
in human infants.121–124 Slack and colleagues118 described pneumothorax and pneu-
momediastinum in a calf born by caesarian section with substantial meconium stain-
ing. The calf was resuscitated with mechanical ventilation, however, so both of these
 Respiratory Disease of the Bovine Neonate 131

could have been contributory. Calves with pneumothorax frequently have dyspnea,
tachypnea, and absent lung sounds in the dorsal lung field. Cattle have a complete
mediastinum, and pneumothorax may be limited to one hemithorax depending on
the inciting cause. Treatment of pneumothorax involves therapy for the primary dis-
ease together with evacuation of air from the pleural space. In the field, suction of
air can be done with a teat cannula or an 18-gauge 3.5-in (51-mm) catheter,
a three-way valve, and a syringe. This procedure may need to be repeated as dictated
by the clinical signs of the calf. Severe, persistent pneumothorax may require hospi-
talization and continuous suction with a device as described by Peek and
colleagues.117
Dyspnea and tachypnea from pulmonary edema or laryngeal edema can occur with
anaphylactic reactions in calves induced by exogenous antigens. Anaphylactic reac-
tions are type 1 hypersensitivity reactions mediated by IgE. Antibiotic therapy with
penicillin G, sulfonamides, tetracyclines, epidural analgesia with lidocaine or Carbo-
caine, and vitamin E and selenium injection have been associated with anaphylactic
reactions in cattle.115 Plasma and other blood products have the potential for anaphy-
laxis and animals receiving transfusions need to be monitored closely. Treatment is
dependent on severity of clinical signs and can include epinephrine (0.01 mg/kg);
corticosteroids (dexamethasone, 0.1–0.2 mg/kg); antihistamines (tripelennamine
hydrochloride, 1 mg/kg IM or SQ); furosemide (0.05–1 mg/kg IM or IV), nonsteroidal
anti-inflammatory drugs (flunixin meglumine, 1.1 mg/kg IM or IV); and nasal adminis-
tration of oxygen.115,117

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