Case Report Rapport de cas
Ruminal acidosis in a 21-month-old Holstein heifer
Helen M. Golder, Pietro Celi, Ian J. Lean
Abstract — Rumen and blood biochemical profiles were monitored in 8 Holstein heifers exposed to a carbohydrate
feeding challenge. One of the heifers had clinical signs consistent with acute ruminal acidosis on the day of, andsubsequent to, the challenge. Within 24 h of challenge, 6 of 7 rumen volatile fatty acids measured were notdetectable in this heifer and her rumen total lactate concentration was . 70 mM.
Résumé — Acidose spumeuse chez une génisse Holstein âgée de 21 mois. Les profils du rumen et del’hématologie biochimiques ont été surveillés chez 8 génisses Holstein exposées à une épreuve d’alimentation en
glucides. L’une des génisses avaient des signes cliniques conformes à une acidose spumeuse aiguë le jour et lelendemain de l’épreuve. Dans un délai de 24 h après l’épreuve, 6 des 7 acides gras volatils du rumen mesurésn’étaient pas détectables chez cette génisse et la concentration de lactate totale de son rumen était de . 70 mM.
(Traduit par Isabelle Vallières)Can Vet J 2014;55:559–564

T

he objective of this report was to describe findings, especially ruminal conditions, that were present in a heifer
with clinical signs consistent with ruminal acidosis. Clinicaldefinitions of ruminal acidosis are inconsistent and largely basedon arbitrary rumen pH cut points (1,2). Lean et al (3) note theneed for definitions of metabolic disease to be accurate, standardized, repeatable, and based on clinical outcomes including
measurable changes in metabolism, morbidity, mortality, or
production.
Sporadic disorders such as acute ruminal acidosis are only
rarely documented in detail that provides a combination of clinical signs, feed intake, nutritional composition of the diet, andrumen and blood measures; therefore, there is merit in presenting observations on a clinical case, particularly when detailed
comparative data on other cattle were available.
We report feed intake, clinical signs, and rumen and bloodbiochemical profiles of a heifer exposed to a diet high in readily
fermentable carbohydrates for 20 d preceding challenge with adiet containing 19.1% sugar and 54.1% starch on a dry mat-

SBScibus, Camden, New South Wales, Australia 2570 (Golder,
Lean); Dairy Science Group, Faculty of Veterinary Science,
University of Sydney, Camden, New South Wales, Australia
2570 (Golder, Celi, Lean); Melbourne School of Land andEnvironment, The University of Melbourne, Parkville, Victoria,
Australia 3010 (Celi).
Address all correspondence to Ms. Helen Golder; e-mail:heleng@sbscibus.com.au
Use of this article is limited to a single copy for personal study.
Anyone interested in obtaining reprints should contact the
CVMA office (hbroughton@cvma-acmv.org) for additional
copies or permission to use this material elsewhere.
CVJ / VOL 55 / JUNE 2014

ter (DM) basis. Her rumen and blood biochemical profiles arecompared to those of 7 cohort heifers.

Case description
A 21-month-old pregnant Holstein heifer [Identification
No. 1250; body weight (BW): 488 kg] showed clinical signsof ruminal acidosis within 10 h of consuming 4.8 kg DM ofmilled wheat and 960 g DM of fructose (1.0 and 0.2% of her
BW, respectively). Heifer 1250 was 1 of 8 control heifers (mean
BW: 382 6 17 kg, excluding heifer 1250) enrolled in a 29 dreadily fermentable carbohydrate challenge study evaluating theeffectiveness of feed additives to reduce acidosis risk (4). The
study was conducted at Cobbitty, New South Wales, Australia.
All experimental procedures were approved by the SBScibus
Animal Ethics Committee (SBScibus 0512-0513).
The study consisted of 5 experimental periods: 1) pre-­adaptation (days 22 to 0), 2) adaptation I (days 1 to 10),3) adaptation II (days 11 to 20), 4) challenge (day 21), and5) post-challenge (days 22 to 26). Rations offered at each ofthese periods are detailed in Figure 1 and Table 1. The 20-day
adaptation period was considered adequate to study rumen perturbation. Rumen and blood samples were not collected fromthe cohort heifers during the post-challenge period. Heifers wererandomly allocated to 1 of 4 blocks (A to D; 2 heifers/block),enrolment of each block of heifers in the study was staggeredover 4 consecutive days. Heifer 1250 was allocated to block A.
All heifers were housed with the main study herd in a paddock containing dormant kikuyu (Pennisetum clandestinum)with no available pasture and ad libitum water access. An equalamount of feed was offered twice daily at 7:00 and 14:00 h inindividual feed bins and separate feeding pens that prevented
access between pens. The amount of ration that the heifers
consumed before ceasing consumption and the time they took559

R A P P O R T D E CA S

Figure 1. Experimental periods and their corresponding study days and rations offered for the study in which heifer 1250 and hercohort of heifers were enrolled.

BW — body weight; DMI — dry matter intake; TMR — total mixed ration (62:38 forage:concentrate, consisting of 31.5% wheaten hay, 30.5% alfalfa hay,and 38% milled wheat).
a Rumen and blood samples were collected on days 0, 7, 14, and 21 during their respective experimental periods from both heifer 1250 and her cohortof heifers.
b Rumen and blood samples were collected from heifer 1250 on days 22 and 23.
c Introductory doses were offered for the initial days before the full rate was offered.

to consume this amount were recorded. Consumption time
did not exceed 2 h. Heifers were subsequently returned to thepaddock with no access to feed until the next feeding session.
Heifer 1250’s dry matter intake (DMI) over the 20-day
adaptation period, in which she was offered 2.5% of her BW
DM total mixed ration (TMR)/d (days 1 to 10) and additional
0.1% of her BW fructose (d 11 to 20), averaged 8.6 kg DM/d(84 6 3.3% of the offered ration/d), compared to 8.3 6 0.3 kg
DM/d (91 6 1.5% of the offered ration/d) for the cohort heifers. Qualitatively, she had a similar DMI pattern to the cohort
heifers, but had more pronounced drops in DMI. She consumed
only 4.9 kg DM/d (50% of her allocated ration) on day 4 anda physical examination showed that her rectal temperature,
rumen contractions, and heart rate (80 beats/min) were within
normal ranges. Her DMI also decreased during the 4 d before
challenge (days 17 to 20), to approximately 9.6 kg DM/d (79%of her offered ration/d), from approximately 11.5 kg DM/d
(95% of her offered ration) for days 13 to 16. On days 17 to
20 the cohort heifers consumed on average 9.3 6 0.3 kg DM/d(95 6 1.5% of their offered ration/d).
Rumen fluid collected using a customized stomach pump andtube, and blood samples were taken weekly before challenge on
day 0 (pre-adaptation), day 7 (adaptation I), and day 14 (adaptation II). The stomach tube was inserted to a minimum lengthof 2 m and rumen fluid was scored for saliva contamination (5).
Rumen pH (Merck, Kilsyth, Victoria, Australia; Figure 2I) was
measured within 3 min of collection of rumen fluid and all othermeasurements were done at a later date on samples immediately
placed on ice and later stored at 220°C. All rumen and bloodmeasures from heifer 1250 were compared with those of the
7 other heifers and are referred to as higher or lower if they areoutside the mean 6 standard error of the mean (SEM) of thesecohort heifers.
Heifer 1250 had a higher rumen pH (Figure 2I), 20 to
30 mM lower total VFA’s, which comprised acetate, propionate, butyrate, valerate, isobutyrate, isovalerate, and caproate
measured by gas chromatography (Figure 2A), lower major
individual VFA’s (Figures 2B, C, E, and F), and a similar acetate
to propionate ratio (Figure 2D) than the cohort heifers before
challenge day. The heifer’s ammonia concentration measured bya direct enzymatic method was lower in the adaptation II sampling (Figure 2G), while her total rumen lactate concentration(D-lactate; Boehringer Mannheim kit: cat no. 11 112 821 035;
R-Biopharm-Laboratory Diagnostics, Taren Point, New South
Wales, Australia; L-lactate; cat no. OSR 6193; Beckman Coulter
560

Australia, Gladesville, New South Wales, Australia) was higher
in the adaptation I sampling (Figure 2H).
Plasma reactive oxygen metabolites (dROMs; d-ROMS Test;
Diacron International, Grosseto, Italy) and biological antioxidant potential (BAP; Bap Test; Diacron International) (6)were increased in heifer 1250 compared to the cohort heifers
at the adaptation I and II samplings, respectively (202 compared to 138 6 14 Carratelli units, and 4351 compared
to 3884 6 280 mmol/L). Heifer 1250’s plasma oxidative
stress index [OSI; (dROMs/BAP) 3 100 (6)] (Figure 2J) was
increased in the pre-adaptation and adaptation I samplings. Her
plasma ceruloplasmin (7) dropped 133.7 mg/L between the pre-­adaptation and adaptation I samplings (Figure 2K).
Serum non-esterified fatty acid (NEFA) concentrations(Randox Laboratories, Crumlin, Antrim, UK) for heifer 1250
were similar to those of the cohort heifers before challenge. Her
serum b-hydroxybutyrate concentration (Randox Laboratories)
was higher in adaptation II than that of the cohort heifers (Figure 2L). Heifer 1250’s serum glucose concentration(InfinityTM Glucose Hexinase Liquid Stable Reagent; Thermo
Scientific, Scoresby, Victoria, Australia) was lower in the adaptation II sampling than that of the cohort heifers (4.3 compared
to 4.8 6 0.2 mM, respectively). Serum urea concentrations forheifer 1250 (InfinityTM Urea Liquid Stable Reagent; Thermo
Scientific) were lower than the cohort heifers’ in the pre-­adaptation (2.5 compared to 3.8 6 0.2 mM, respectively)
and higher in the adaptation II samplings (5.2 compared to
3.1 6 0.1 mM, respectively).
Heifers were scored for locomotion using a 5-point scoring
system (8) after rumen and blood collection and heifer 1250
was scored as , 2 (sound) during all scoring sessions leading
up to challenge day, similar to her cohorts.
On the challenge day (day 21) each heifer was offered 200 gof alfalfa hay and immediately after its consumption eachheifer was offered 1.0% and 0.2% of their BW DM in milled
wheat and fructose, respectively, and 200 g of wheat pellets.
The challenge ration had 19.1% DM sugar and 54.1% DM
starch content (CPM Dairy Analyzer V3.10; Cornell-PennMiner, Cornell University, Ithaca, New York, USA; Table 1).
Feeding was staggered within each block with the first heifer
fed at 7:00 h. Heifer 1250 consumed 100% of her offered
4.8 kg DM of milled wheat, 960 g DM of fructose, and 200 gof wheat pellets in 36 min (total intake 6.0 kg DM). The mean
DMI, percentage of offered ration consumed, and consumption
time for the cohort heifers were 4.2 6 0.4 kg DM, 90 6 9.6%
CVJ / VOL 55 / JUNE 2014

Item (% DM)
DM
CP
RUP (% of CP)
RDP (% of CP)
RDP
Soluble protein (% of CP)
ADF
NDF
Forage NDF (% of NDF)
Forage NDF (% of DM)
Physically effective NDF
LigninNFCb
Silage acids
Sugar
StarchSoluble fiber
Total ether extract
Total LCFAAshDCAD (mEq/100 g)
Minerals (mg/kg)
Chloride
Calcium
CopperIron
Phosphorus
Potassium
Magnesium
Manganese
SodiumSulfurZinc

Adaptation I(days 1 to 10)

Adaptation II(days 11 to 20)

Challenge(day 21)

89.6
13.4
27.6
72.4
9.70
39.8
22.4
35.0
85.8
30.0
30.6
3.6
46.1
0.0
9.4
27.5
9.1
1.95
1.39
5.98
24.7

89.9
14.1
21.3
78.7
11.1
45.0
21.6
33.6
85.8
28.8
29.4
3.5
47.7
0.0
12.6
26.4
8.7
1.88
1.34
4.94
23.7

90.2
9.8
11.8
88.2
8.60
38.5
4.49
10.7
0.0
0.0
4.2
0.9
76.3
0.0
19.1
54.1
3.2
1.74
1.57
1.82
20.25

4400
4800
21
128
3000
1700
1400
75
1300
1900
64

4300
4500
19
122
2900
16 300
1300
70
1200
1800
58

1000
900
20
42
2800
4100
1000
58
100
1300
62

a Estimations were performed using CPM Dairy Analyzer V3.10 (Cornell-Penn-Miner,

Cornell University, Ithaca, NY, USA).

b NFC = 100 — [(NDF — NDICP) 1 CP 1 crude fat 1 ash].

DM — dry matter, DMI — dry matter intake, TMR — total mixed ration, CP —crude protein, RUP — rumen undegradable protein, RDP — rumen degradable
protein, ADF — acid detergent fiber, NDF — neutral detergent fiber, NFC — nonfiber carbohydrates, LCFA — long-chain fatty acids, DCAD — dietary cation-anion
difference.

and 62 6 9.8 min, respectively. At approximately 3.6 h after
consumption of the ration a rumen fluid sample and a blood
sample were collected from all heifers.
Heifer 1250’s rumen pH was 5.1 on the challenge day, which
was a decline of 1.7 pH units from her pre-adaptation sample
pH. Mean rumen pH of the cohort heifers on the challenge day
was 5.7 (Figure 2I).
On the challenge day heifer 1250’s total VFA concentration was
lower (82.9 mM) compared with her cohorts (114.7 6 13.4 mM;
Figure 2A). Her acetate concentration was similar to the cohort
heifers’ (Figure 2B); however, her propionate concentration was
lower at 7.7 mM compared with 24.1 6 4.1 mM for her cohorts(Figure 2C), and her acetate to propionate ratio was 8.2 comparedwith 3.1 6 0.4. Heifer 1250’s butyrate concentration was lower
CVJ / VOL 55 / JUNE 2014

(10.7 mM) than the cohort heifers’ (19.3 6 3.6 mM; Figure 2E).
Her valerate concentration was lower at 0.5 mM compared with
3.0 6 0.9 mM for the cohort heifers (Figure 2F), and ammonia
concentration was over 6-fold higher than that of the cohort heifers (Figure 2G).
Heifer 1250’s rumen histamine concentration (human histamine ELISA kit; IBL International, Hamburg, Germany) was
more than double that of the cohort heifers’ on challenge day,
291.6 and 124.2 6 40.5 mM, respectively. Her dROMs werehigher over the challenge period than that of the cohort heifers (147 compared to 120 6 10 Carratelli units) and her OSI
measure was 4.1 compared to 3.4 6 0.4 for the cohort. Her
ceruloplasmin concentrations were lower (157.5 mg/L) thanthose of the cohort heifers (247.1 6 43.2 mg/L; Figure 2K).
Heifer 1250’s b-hydroxybutyrate (Figure 2L) and urea concentrations were higher than those of the cohort heifers on thechallenge day (4.1 compared to 2.9 6 0.3 mM, respectively),while her glucose was lower (3.7 and 4.8 6 0.3 mM, respectively) and her NEFA was similar (0.07 and 0.05 6 0.02 mM,
respectively).
In the afternoon after the challenge all heifers were scored forlocomotion and offered ad libitum access to wheaten and millet
hay 7 h after the challenge with close monitoring of feed intake.
Heifer 1250’s locomotion score was 1.5, compared to 1.1 6 0.1
for the cohort heifers.
The first clinical sign that heifer 1250 may have had acuteruminal acidosis was a different behavior from her cohort heifers when hay was offered. The cohort heifers rushed to eat thehay, whereas heifer 1250 showed no interest in eating. At 17:30,
20:00, and 22:30 h checks she stood at the rear of the paddock,continued to show no interest in hay, had very loose diarrhea,
and had dull mentation, but was sufficiently alert to not allow
contact within 3 m.
On the morning after challenge (day 22), heifer 1250 stoodin an area surrounded by watery, bubbly diarrhea, was dull,
and walked tentatively. Her heart rate was 66 beats/min, respiration rate was 18 breaths/min, and her rumen was staticand distended, as assessed by auscultation and ballotment of
the paralumbar fossa. Rumen fluid and a blood sample weretaken at 7:00 h and the immediate rumen pH measure was
5.5. Later VFA analysis (in duplicate) revealed heifer 1250
had no detectable concentrations of propionate, butyrate,
valerate, isobutyrate, isovalerate, or caproate (Figure 2 C,E,F).
The only VFA detected was 15.2 mM acetate (Figure 2B). Her
ammonia concentration was 13.5 mM (Figure 2G) and total
rumen lactate concentration was 67% (70 mM; Figure 2H)
and rumen histamine concentration was 77% (224 mM), of therespective concentrations measured 20 h earlier. Her OSI had
returned to a similar level to that reported at the adaptation II
sampling (Figure 2J), but plasma ceruloplasmin was 266 mg/L
(Figure 2K). Heifer 1250’s b-hydroxybutyrate concentration
was approximately 6-fold lower than 20 h earlier (Figure 2L).
Her NEFA concentration was 58% higher, and her urea andglucose were approximately 53 and 9% lower, respectively, than
20 h earlier.
Heifer 1250 was treated by stomach tube with 200 g of
sodium bicarbonate (Penice Soda Products; Osborne, South
561

CA S E R E P O R T

Table 1. Estimated chemical composition of the ration offeredduring the following periods: 1). adaptation I [comprising 2.5%of body weight (BW) DMI/d total mixed ration (TMR) 1 200 g/d
wheat pellets], 2). adaptation II (comprising 2.5% of BW DMI/d
TMR 1 0.1% of BW/d fructose 1 200 g/d wheat pellets), and
3). challenge (comprising 1.0% of BW DMI wheat 1 0.2% of BW
fructose 1 100 g wheat pellets)a. Estimations were based on a
400 kg BW heifer with a body condition score of 3.25 and a
growth rate of 0.73 kg/d. The TMR (62:38 forage:concentrate)consisted of 31.5% wheaten hay, 30.5% alfalfa hay, and 38% discmilled wheat

R A P P O R T D E CA S

Figure 2. Ruminal total volatile fatty acid (VFA) (A); acetate (B); propionate (C); acetate:propionate (D); butyrate (E); valerate (F);ammonia (G); and total lactate (H); concentrations, and pH (I); plasma oxidative stress index (OSI) (J); plasma ceruloplasmin (K); andserum b-hydroxybutyrate (L) concentrations in heifer 1250 that was diagnosed with acute ruminal acidosis and the mean (6 SEM) of
7 cohort heifers. Rumen fluid samples were collected using a stomach tube over the following 5 experimental periods on the study day
indicated in parentheses: Pre — pre-adaptation (d 0); AI — adaptation I (d 7); AII — adaptation II (d 14); Chall — challenge (d 21); andPC — post-challenge (days 22 and 23). Refer to Figure 1 for rations offered during each experimental period. On challenge (day 21)
rumen fluid samples were collected approximately 3.6 h after the challenge rations were consumed. *Rumen fluid was not collectedfrom the 7 cohort heifers during the post-challenge period.
562

CVJ / VOL 55 / JUNE 2014

Discussion
The clinical signs of diarrhea, inappetence, and reluctance tomove observed within 10 h of consumption of readily fermentable carbohydrate are consistent with the diagnosis of acuteruminal acidosis (1). Total lactic acid concentrations were within
the range for acute acidosis (2), throughout the challenge andremained within this range 1 d after, until these returned tonear zero 2 d after challenge. When considering the difference
between rumen pH values collected by stomach tube and fistula,
the observed pH of 5.1, 3.6 h after challenge ration consumption is consistent with acute acidosis definitions (9). However,rumen pH was 5.5 when the clinical signs were observed. It is
possible rumen pH continued to decline after 3.6 h; however,rumen fluid collection at 2 to 5 h after the primary concentratemeal has been reported as the optimum sampling time (10) andsymptoms were most visible at the time pH was 5.5.
This is the first reported case in cattle, in which the individual VFA’s, propionate, butyrate, isobutyrate, isovalerate,
CVJ / VOL 55 / JUNE 2014

valerate, and caproate, were not detected during clinical ruminal
acidosis. An absence of propionate and butyrate concentrations
was similarly noted in wethers within 14 h of being administered a sucrose solution at 15 g/kg BW through a rumen
fistula (11). Further, all wethers had acetate concentrations of, 5 mM within 24 h of treatment and lactate concentrations
were . 70 mM (11). No detectable or very low concentrationsof propionate, acetate, and valerate were reported in sheep asearly as 10 h after 1.4 to 2.7 kg of cracked wheat was administered through a rumen fistula (12). A total VFA concentrationof , 20 mM was reported in a wether 24 h after consuming
6.8 kg of mangolds (13). It has been suggested that in acuteacidosis, VFA concentrations are initially increased and thendecline below 100 mM (2); however, these observations suggest
a more dramatic decline is present.
This study was planned to induce an acidosis of non-lifethreatening severity based on feeding an amount of grainsimilar to percentages that are commonly fed to beef and dairy
cattle and 0.2% of BW DMI of fructose which was designed
to increase the risk of acidosis and mimic large exposures tosugar sources from access to high fructan or sucrose sources
such as some fresh forages, brassicas, or citrus pulp, molasses,
whey, or crystalline sugar. The fructose would have been rapidly
fermented and may have increased rumen fluid passage andhindgut fermentation. Thus, grain fed in the milking parlour in
combination with sugar sources and inadequate effective fiber
may place cattle at increased risk of acidosis.
Individual animals have different susceptibilities to acidosis(14). Heifer 1250 had a different rumen fermentation profile
to her cohorts at study day 0 which may indicate an inherent
increased risk of acidosis. Her reduction in DMI to approximately 9.6 kg DM/d (79% of her offered ration/d) during
the 4 d leading up to the challenge day may further indicate
a greater susceptibility to acidosis compared with the cohort
heifers before challenge. Her rapid consumption of 100% of
the ration in approximately half the time of the cohort heifers
may have also increased her risk of acidosis. As a consequenceof heifer 1250 developing acidosis, the 6 heifers allocated toblocks B to D that were challenged on subsequent days were
drenched with 200 g of sodium bicarbonate 4 h after thechallenge.
Bramley et al (5) defined acidosis on the basis of a combination of individual VFA’s, ammonia, rumen pH, and lactate
measures. Definitions based on rumen pH cut points alone
are not consistent and need to be accurately defined to allow
appropriate diagnosis and treatment. Definitions also need to
be specific for rumen fluid collection method to account for
the heterogeneous nature of the rumen and also need to betteraccommodate single samples. This case study supports the workof Bramley et al (5) suggesting that rumen pH is not the key
indicator of acidosis. Although heifer 1250 had lower rumen
pH values than the cohort heifers, her pH was borderline fordiagnosis of acute acidosis, whereas the very high lactate, andhistamine and low VFA levels were suggestive of acute acidosis.
This suggests that high rumen lactate concentrations do not necessarily correspond to a very low rumen pH and cowside VFA
tests may be important diagnostic tools for acidosis in the future.
563

CA S E R E P O R T

Australia, Australia) in 20 L of water at 7:30 h (d 22), before
being scored for locomotion. She was reluctant to walk; her gait
was slow and tentative and was scored at 2.5, 1 score higher thanthe previous day. No other heifers in the cohort had locomotion
scores greater than 1.5. Heifer 1250 was housed in a separate yard
where she was offered wheaten and millet hay and water, noneof which she consumed. Later she was offered TMR but there
was no detectable intake. She was given Flunixin meglumine(Ilium Flunixil; Troy Laboratories, Smithfield, New South Wales,
Australia), 2.2 mg/kg BW, IM, at 14:30 h on the same day. She
was examined on day 23, 48 h after challenge. At this time herappetite had resumed and she displayed no abnormal signs during a physical examination. She was subsequently returned tothe main herd. Rumen fluid and blood measures from samples
collected at 14:00 h on the same day (day 23) revealed that her
total VFA concentrations had returned to a similar concentration
to those on the challenge day. Her acetate to propionate ratio(Figure 2D) was 2.2, valerate concentration was much higher(2.77 mM) than her previous recordings (Figure 2F), ammonia
had dropped markedly to 0.53 mM (Figure 2G), and total lactate
concentration was very low (Figure 2H). Her rumen histamine
concentration had decreased from the previous sampling by 70%,
OSI increased by 21% (Figure 2J), BAP decreased by 15%, andplasma ceruloplasmin had decreased dramatically from 265.9
to 40.0 mg/L (Figure 2K). Heifer 1250’s NEFA concentrations
decreased from 0.17 to 0.09 mM, while her b-hydroxybutyrate(0.15 to 0.40 mM; Figure 2L), glucose (3.4 to 4.1 mM), andurea concentrations (1.9 to 2.7 mM) increased compared tothe previous day. Her DMI (11.1 6 1.1 kg DM; 91 6 9.4%of offered ration) on the 2nd and 3rd day after challenge wassimilar to the cohort heifers’ (8.9 6 0.6 kg DM; 91 6 6.2% ofoffered ration). Her locomotion score was normal on day 26 andconsistent with that of the cohort heifers.
Over the study, heifer 1250 gained 34 kg BW and on average
the cohort heifers gained 37 6 4 kg BW. After being returnedto the farm of origin heifer 1250 calved with no complications
and the herd manager reported that she has been in excellent
health since her return.

R A P P O R T D E CA S

The increases in histamine were consistent with the knowledge that histamine generation occurs after feeding and canaccumulate in the rumen during acidotic conditions (15,16).
The increase in locomotion score suggests an association withhistamine. While net absorption of histamine from the rumen
appears to be low, and it is inactivated either during or after
absorption into the blood, low rumen pH, and gut lesions may
favor absorption (17).
The increase in OSI after challenge suggests heifer 1250 was
subject to increased oxidative damage, an observation whichis consistent with elevated oxidative stress measures in cattle
fed high starch diets (18). The decrease in ceruloplasmin and
BAP concentrations 2 d after the challenge may suggest they
are involved in the pathogenesis of acidosis (19). The decreasein b-hydroxybutyrate, glucose, and urea and increase in NEFA
concentrations 24 h after challenge support the presence of ametabolic disturbance. These measures may also be useful ancillary diagnostic measures for acidosis that could be developed forcowside use in the future.
In conclusion, this study emphasizes the variability in susceptibility to acidosis of individual cattle and the importanceof detection of early clinical signs such as decreases in DMI,
diarrhea, and change in demeanor. It also draws attention to thepotential dangers of sugars in the diet, particularly in combination with grain. Clinicians should be aware that rumen pH is
not always an adequate diagnostic method for evaluating acidosis, especially when a single sample is obtained. Other rumen
measures including rumen VFA, lactic acid, and ammonia canprovide a greater understanding of rumen function. Recovery of
rumen function can occur rapidly after treatment despite severe
perturbation.
CVJ

References
1. Plaizier JC, Krause DO, Gozho GN, McBride BW. Subacute ruminal
acidosis in dairy cows: The physiological causes, incidence and consequences. Vet J 2008;176:21–31.
2. Nagaraja TG, Titgemeyer EC. Ruminal acidosis in beef cattle: The
current microbiological and nutritional outlook. J Dairy Sci 2007;90:
E17–E38.

564

3. Lean IJ, Rabiee AR, Duffield TF, Dohoo IR. Invited review: Use ofmeta-analysis in animal health and reproduction: Methods and applications. J Dairy Sci 2009;92:3545–3565.
4. Golder HM, Celi P, Rabiee AR, Lean IJ. Effects of feed additives on
rumen and blood profiles during a starch and fructose challenge. J Dairy
Sci 2014;97:985–1004.
5. Bramley E, Lean IJ, Fulkerson WJ, Stevenson MA, Rabiee AR, Costa
ND. The definition of acidosis in dairy herds predominantly fed on
pasture and concentrates. J Dairy Sci 2008;91:308–321.
6. Celi P. Biomarkers of oxidative stress in ruminant medicine. Immuno­
pharmacol Immunotoxicol 2011;33:233–240.
7. Sunderman FW, Jr. Nomoto S. Measurement of human serum ceruloplasmin by its p-phenylenediamine oxidase activity. Clin Chem 1970;
16:903–910.
8. Sprecher DJ, Hostetler DE, Kaneene JB. A lameness scoring system thatuses posture and gait to predict dairy cattle reproductive performance.
Theriogenology 1997;47:1179–1187.
9. Duffield T, Plaizier JC, Fairfield A, et al. Comparison of techniques formeasurement of rumen pH in lactating dairy cows. J Dairy Sci 2004;
87:59–66.
10. Nordlund KV, Garrett EF. Rumenocentesis: A technique for collecting
rumen fluid for the diagnosis of subacute rumen acidosis in dairy herds.
Bovine Pract 1994;28:109–112.
11. Kezar WW, Church DC. Ruminal changes during the onset and recovery of induced lactic acidosis in sheep. J Anim Sci 1979;49:1161–1167.
12. Ryan RK. Concentrations of glucose and low-molecular-weight acidsin the rumen of sheep following the addition of large amounts of wheat
to the rumen. Am J Vet Res 1964;25:646–652.
13. Scarisbrick R. Acid indigestion in a sheep fed on mangolds. Vet Rec
1954;66:131–132.
14. Brown MS, Krehbiel CR, Galyean ML, et al. Evaluation of models of
acute and subacute acidosis on dry matter intake, ruminal fermentation, blood chemistry, and endocrine profiles of beef steers. J Anim Sci
2000;78:3155–3168.
15. Golder HM, Celi P, Rabiee AR, et al. Effects of grain, fructose andhistidine on ruminal pH and fermentation products during an induced
subacute acidosis protocol. J Dairy Sci 2012;95:1971–1982.
16. Ahrens FA. Histamine, lactic acid and hypertonicity as factors in thedevelopment of rumenitis in cattle. Am J Vet Res 1967;28:1335–1342.
17. Aschenbach JR, Gabel G. Effect and absorption of histamine in sheep
rumen: Significance of acidotic epithelial damage. J Anim Sci 2000;
78:464–470.
18. Gabai G, Testoni S, Piccinini R, Marinelli L, Stradaioli G. Oxidative
stress in primiparous cows in relation to dietary starch and the progressof lactation. Anim Sci 2004;79:99–108.
19. Celi P. Oxidative stress in ruminants. In: Mandelker L, Vajdovich P,
eds. Oxidative Stress in Applied Basic Research and Clinical Practice.
New York, New York: Humana Press, 2011:191–231.

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