International Journal of Veterinary Science and Medicine xxx (2017) xxx–xxx

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International Journal of Veterinary Science and Medicine

journal homepage: www.elsevier.com/locate/ijvsm
www.vet.cu.edu.eg

Short Communication

Field evaluation and confirmation of acute peste des petits ruminant

outbreak in a flock of West African dwarf goats in Ibadan, Nigeria
Balogun F. Adeola a, Fasanmi O. Gabriel a,b,⇑, Oladipo T. Ademola a, Popoola M. Abiola a,
Olona J. Folami a, Adeoye Y. Dorcas a
a
Federal College of Animal Health and Production Technology, Moor Plantation, Ibadan, Nigeria
b
Department of Production Animal Studies, Faculty of Veterinary Science, University of Pretoria, Onderstepoort, South Africa

a r t i c l e i n f o a b s t r a c t

Article history: This study utilised epidemiological, haematological, pathological findings and serological detection of
Received 12 July 2017 specific antibodies to evaluate and confirm a peste des petit ruminants (PPR) outbreak in a herd of west
Revised 18 August 2017 African dwarf (WAD) goats in Ibadan, Nigeria. The morbidity and mortality rates post exposure (PE) were
Accepted 29 August 2017
96% and 60% respectively. Laboratory analyses revealed significant differences (P < 0.05) in mean values
Available online xxxx
of the haematological and serum biochemical indices between the PE and control groups. The PE group
experienced a significant (P < 0.05) increase in white blood cell (WBC), lymphocyte and monocytes after
Keywords:
10 days PE; the drop in glucose and high levels of alkaline phosphatase (ALP) and aspartate amino trans-
Haematology
Morbilli virus
ferase (AST) indicated liver damage, while increased serum creatinine, blood urea nitrogen (BUN) and
Peste des petit ruminant uric acid arose from kidney impairment. The electrolyte imbalance (potassium, sodium and chloride ions)
Post exposure resulting from the symptomatic diarrhea affected the functionality of the Na+–K+ pump mechanisms,
Serum biochemistry hence pathologic damage to the liver, kidneys, skin, gastrointestinal, respiratory and cardiovascular sys-
West African dwarf goat tems.
The competitive enzyme linked immuno-sorbent assay (c-ELISA) detected varying antibody levels in
the PPR infected WAD goats; the percent inhibition was highest (P < 0.001) in survivors (70.00 ± 1.73),
then in contact group (60.00 ± 2.00), and least in infected (23.33 ± 1.53), which were sero-negative.
This study confirmed a PPR outbreak in a WAD goat flock in Ibadan, Nigeria.
Ó 2017 Faculty of Veterinary Medicine, Cairo University. Production and hosting by Elsevier B.V. This is an
open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

1. Introduction contaminated feed or water. Secretions and excretions of sick ani-

mals are the sources of infection, which can also occur during the
Peste des petits ruminants (PPR), also referred to as ovine incubation period [7]. The PPR is characterized by a sudden onset
rinderpest, goat plague, plague of small ruminants, Kata or of depression, fever, discharges from the eyes and nose, sores in
stomatitis-pneumoenteritis complex; is an acute, highly conta- the mouth, disturbed breathing, coughing and foul-smelling
gious and infectious viral disease of small ruminants, which is clo- diarrhoea. The morbidity and mortality rates can be as high as
sely related antigenically to rinderpest in goats and sheep [1]. The 90–100% in virgin populations, dropping to about 20–40% in ende-
disease was first confirmed in Cote d’Ivoire, West Africa in 1942, mic areas [2,3]. The disease was first reported in Nigeria between
and endemic to most of Saharan and sub-Saharan Africa, Turkey, 1950 and 1960, and thereafter outbreaks have been reported
the Middle East and the Indian subcontinents [2–4]. The PPR is a across the country on a yearly basis. The epidemiology of PPR in
notifiable disease on account of the rapidity of its spread, high Nigeria has not been fully elucidated; and it is possible that it
morbidity and mortality [5,6]. Transmission is mainly through occurs in a more diverse range of hosts [8,9]. It has become a major
aerosols between animals living in close contact, and confinement threat to small ruminant existence and food security in Africa and
seems to favour outbreaks, but it may also happen by feeding of neighbouring continents [10]. Vaccination remains the most effec-
tive and viable tool for the prevention of this infection, but the vac-
cines are relatively scarce [6,7].
Peer review under responsibility of Faculty of Veterinary Medicine, Cairo
University.
This study utilised the epidemiological, clinical, haematological,
⇑ Corresponding author at: Department of Production Animal Studies, Faculty of pathological findings and serological detection of specific antibod-
Veterinary Science, University of Pretoria, Onderstepoort 0110, South Africa. ies to evaluate and confirm PPR outbreak in WAD goats.
E-mail addresses: 15340482@tuks.co.za, bumaetal@gmail.com (O.G. Fasanmi).

https://doi.org/10.1016/j.ijvsm.2017.08.004
2314-4599/Ó 2017 Faculty of Veterinary Medicine, Cairo University. Production and hosting by Elsevier B.V.
This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

Please cite this article in press as: Balogun FA et al. Field evaluation and confirmation of acute peste des petits ruminant outbreak in a flock of West African
dwarf goats in Ibadan, Nigeria. Int J of Vet Sci Med (2017), https://doi.org/10.1016/j.ijvsm.2017.08.004
2 F.A. Balogun et al. / International Journal of Veterinary Science and Medicine xxx (2017) xxx–xxx

2. Materials and methods The paired sera samples were analysed for the presence of PPRV
specific antibodies using an anti- nucleocapsid monoclonal anti-
2.1. Study location and study animals body (MAb) based competitive ELISA (c-ELISA) [16]. ELISA plates
(NUNCMaxisorp, Hamburg, Germany) were coated with the PPRV
The PPR outbreak; occurred at the student research farm unit of antigen (50 lL/well) incubated at 37°C for 1 h; thereafter the wells
the Federal College of Animal Health and Production Technology, were washed three times with 0.002 mol/L phosphate-buffered
Moor Plantation, Ibadan, South Western Nigeria (7° 240 300 N, 3° saline (PBS) before 40 lL of blocking buffer (PBS with 0.2% PPR-
510 900 E). The location is in a tropical rainforest-derived savannah negative goat serum and 0.1% Tween 20) was added to each well.
transition zone with an average relative humidity of 75–90% and Twenty lL of the test samples were added to duplicate sets of
mean monthly temperature range of 26–28°C. There are two main wells, followed by addition of 40 ll of MAb in each well with the
seasons, with the rain season spanning from April to October and exception of conjugate control wells, at a final dilution of 1:500.
the dry season from November to March. The study animals were Anti-mouse–HRPO conjugate (Dako, Glostorp, Denmark) diluted
25 apparently healthy female WAD goats between 6 and 8 months 1:1000 in blocking buffer was added to each well (50 lL/well) after
of age, purchased for research purposes, that were sourced from incubation. Finally, substrate solution orthophenylene diamine
different locations and local livestock markets in Offa, Kwara State, (OPD) was added to each well and the colour reaction allowed to
Nigeria, about 170 km from Ibadan. The animals were kept in a develop for 10 min before the reaction was halted with 1 mol/L
well constructed ruminant holding units, intensively managed H2SO4. Optical density (OD) was measured at a wavelength of
and placed on basal diets (grasses, legumes and concentrates). Ani- 492 nm.
mals were allowed to acclimatise prior to the date for the com-
mencement of the initially planned research. During this period 2.4. Post-mortem examination
ectoparasitic treatment and deworming were carried out. Prelimi-
nary haematological analysis was carried out and the results Post-mortem examination was carried out in 4 freshly dead
served as control samples. After the acclimatization period, the goats with clinical symptoms of PPR.
PPR outbreak occurred. It started in April 2017 and ended in June
2017.
2.5. Statistical analysis
2.2. Haematology and biochemistry
All the data generated from this study (haematological and
Five mL of blood per goat were collected by jugular venipunc- serum biochemical from blood and sera respectively, and percent-
ture using a sterile 5 mL needle and hypodermic syringe. Two mL age inhibition from c-ELISA) were subjected to analysis of variance
of blood were put into a labelled tube containing EDTA anticoagu- (ANOVA) [17]. If significant differences occurred, the means were
lant, while 3 mL were put in tubes without anticoagulant. The first separated by Duncan multiple range test (DMRT). The results were
set of blood samples were collected prior to the outbreak of PPR, presented as mean with the standard error and P-value < 0.05 was
and subsequent blood collections were undertaken10 days and considered significant.
15 days post exposure. Haematological and serum biochemical
analyses were carried out at the laboratory of Department of 3. Results
Veterinary Physiology, University of Ibadan, Nigeria. Blood samples
were analysed for hematological parameters; packed cell volume 3.1. History, epidemiological and field observations
(PCV), haemoglobin concentration ([Hb]), red blood cell (RBC),
white blood cell (WBC), mean corpuscular volume (MCV), mean There was no record or any history of vaccination against PPR
corpuscular haemoglobin (MCH), lymphocyte (LYM) and serum for any of the goats. An epidemiological survey revealed that there
biochemical parameters and electrolytes (albumin, globulin, have been previous PPR outbreaks in the same locality as the study
creatinine, ALT, AST, blood urea nitrogen, sodium, potassium and location. Also the morbidity rate was 96%. However, 15 out of 25
chloride). Haemoglobin concentration was determined spec- goats died during the outbreak with a mortality rate of 60% (Figs. 1
trophotometrically, as previously described [11], PCV and RBC and 2).
counts were determined as described by Dacie and Lewis [12].
Total WBC counts were determined using Neubauer haemocy-
tometer. Blood constants (MCV and MCH) were determined using 50
appropriate formulae as previously described [13]. The second sets
of samples without EDTA were centrifuged and serum decanted for 45
serum biochemical analysis. Total serum protein was determined 40
using appropriate kits with basic reported procedure [14], albumin 35
was measured using bromocresol green (BCG) binding technique
Mortality (%)

30
as described [15]. Electrolytes (sodium, potassium and chloride)
were determined with an IDEXX Vetlyte Electrolyte and blood R 25
gas analyzer. 20
15
2.3. Serology
10
Blood samples (2.5 mL /goat) were collected by venipuncture 5
into sample bottles without anticoagulant. Sampling was per-
0
formed 10 days post exposure for the PPR infected animals and
1 2 3 4 5 6 7 8 9 10
40 days post exposure for survivors and in contact WAD goats.
PPR Post Infecons (Days)
The samples were transported cooled to a private laboratory in Iba-
dan metropolis for analysis. At the laboratory the sera were sepa-
rated further by centrifugation. Fig. 1. Mortality of WAD goats infected with PPR.

Please cite this article in press as: Balogun FA et al. Field evaluation and confirmation of acute peste des petits ruminant outbreak in a flock of West African
dwarf goats in Ibadan, Nigeria. Int J of Vet Sci Med (2017), https://doi.org/10.1016/j.ijvsm.2017.08.004
 F.A. Balogun et al. / International Journal of Veterinary Science and Medicine xxx (2017) xxx–xxx 3

120
nasal discharges, depression, anorexia and swollen lips. The
affected animals showed signs of severe dehydration and the
100 hindquarters were pasted with diarrhoea. The mouth lesions
were found in all the affected animals with eroded areas on
80 outer and inner side of the lips, lower gums, and necrosis of
Morbidity (%)

the dorsal surface of the tongue. There was a whitish membra-

60 nous covering all over the buccal cavity, and stomatitis was
observed (Fig. 3a–c).
40

20 3.3. Haematological and serum biochemical findings

0
There were significant differences (P < 0.05) in the haemato-
0 2 4 6 8 10 12
logical indices between pre-infection and post-exposure to PPR
PPR Post Infecons (Days)
among the WAD goats (Table 1). Goats tested before infection
with PPR exhibit relatively high values of PCV, [HB], RBC, MCV,
Fig. 2. Morbidity of WAD goats infected with PPR. MCH, neutrophil and eosinophil compared to goats that were
infected and tested after 10 and 15 days. Goats that were infected
3.2. Clinical findings and tested after 15 days had highest values of WBC, lymphocytes
and monocytes (P < 0.05). There were significant differences
During the clinical examination, the affected animals were (P < 0.05) in the serological indices between pre-infection and
coughing, dyspneic and pyrexic, (temperature between 39°C post exposed WAD goats to PPR (Table 2). Pre-infected goats with
and 42°C). Other signs and symptoms included conjunctivitis, PPR exhibit relatively high values of total protein (TP), albumin,

b c

Fig. 3. (a). Goats affected with PPR showing nasal discharges and erosion of the lips; (b). Diarrhoea (faecal pasting of perianal region and hind limbs; (c). Terminal nodular
lesions around the mouth.

Please cite this article in press as: Balogun FA et al. Field evaluation and confirmation of acute peste des petits ruminant outbreak in a flock of West African
dwarf goats in Ibadan, Nigeria. Int J of Vet Sci Med (2017), https://doi.org/10.1016/j.ijvsm.2017.08.004
4 F.A. Balogun et al. / International Journal of Veterinary Science and Medicine xxx (2017) xxx–xxx

Table 1
Haematological indices of WAD Goats naturally infected by PPR.

Parameters Pre-infection Day 10 PE Day 15 PE SEM (±) Normal value (range)*

a b c
PCV (%) 29.33 22.00 15.50 2.01 21–35
[Hb] (g/dL) 10.50a 7.20b 5.70c 0.72 7–15
RBC Count (106/mL) 11.00a 9.50b 6.80c 0.62 9.2–13.5
MCV (fl) 117.10a 95.5b 83.40c 4.93 107.1–121.9
MCH (pg) 38.53a 30.00b 25.00c 1.99 35.6–40.0
WBC Count (103/mL) 12.20c 15.8b 18.90a 0.97 6.8–20.1
Lymphocyte (%) 54.03b 55.40b 57.80a 0.59 47–82
Neutrophils (%) 45.20a 43.70a 41.20b 0.61 17–52
Eosinophils (%) 0.40a 0.20b 0.20b 0.03 1–7
Monocytes (%) 0.40c 0.70a 0.80a 0.06 0–1

PE: Post Exposure.

a,b,c
Means along the same row with different superscripts are statistically significant (P < 0.05).
*
[18,19].

Table 2
Serum biochemical indices of WAD Goats naturally infected by PPR.

Parameters Pre-infection Day 10 PE Day 15 PE SEM (±) Normal value (range)*

a b c
Total protein (g/dL) 7.87 6.40 5.17 0.39 6.8–8.5
Albumin (g/dL) 3.63a 2.97b 1.90c 0.26 2.8–4.3
Globulin (g/dL) 4.23a 3.33b 3.27b 0.16 NA
Creatinine (mg/dL) 1.20c 1.97b 2.90a 0.25 0.50–1.35
Blood Urea Nitrogen (mg/dL) 13.70c 14.80b 16.50a 0.41 15.0–17.0
Uric acid (mg/dL) 2.80c 3.13b 4.33a 0.24 NA
Glucose (mg/dL) 54.83a 48.17b 43.30c 1.69 NA
Potassium (mmol/L) 8.50a 5.80b 4.23c 0.63 3.0–6.0
Sodium (mmol/L) 139.17a 111.40b 84.60c 7.87 124.0–146.0
Chloride (mmol/L) 145.00a 128.00b 115.00c 2.89 NA
AST (IU/L) 15.33c 17.17b 35.17a 3.17 12.0–38.0
ALP (IU/L) 10.67b 12.60a 13.00a 0.25 1.4–24.7

NA: Not Available.

PE: Post Exposure.
a,b,c
Means along the same row with different superscripts are statistically significant (P < 0.05).
*
[18,20].

Table 3
Percentage Inhibition of sera for different categories of WAD goats exposed to PPR infection.

S/N Category of Goat Time sera collected Average Percent Inhibition (%)±SD P-Value
1 Infected (n = 3) 10 days PE 23.33 ± 1.53c
2 Survivor (n = 3) 40 days PE 70.00 ± 1.73a <0.0001
3 In contact (n = 2) 40 days PE 60.00 ± 2.00b

PE: Post Exposure

a,b,c
Means in the same column with different superscripts are statistically significant (P < 0.05).

globulin, glucose, potassium, sodium and chloride compared to 3.5. Detection of PPR antibodies
goats infected with PPR and tested after 10 and 15 days. Goats
infected with PPR and tested after 15 days had highest values Specific antibodies for small ruminant morbilli virus were
of creatinine, blood urea nitrogen, uric acid, potassium, ALP and detected in all the eight paired sera samples collected from WAD
AST. goats in the flocks that experienced the outbreak, following the
usage of PPR c-ELISA kit, sero-positivity and sero-negativity were
3.4. Post-mortem findings determined through the values of percent inhibition (PI). The anti-
body level differed significantly among the PI sera values for the
There were different degrees of erosion and necrosis, and nodu- three categories of infected WAD goats (infected, survivor and in
lar lesions on the lips depending on the stage of infection. At contact /un-infected). Any sera with PI  40% is considered positive
necropsy, internal examination revealed varying degrees of ero- for the presence of PPRV antibodies, while the reverse is the case
sions and necrosis, and a whitish membranous covering lining for PI < 40%. This result however, shows that the survivors had
the buccal cavity and oesophagus. The lungs appeared heavy and the highest antibody titre due to a PI (70 ± 1.73), followed by the
dark (pneumonic lesions) with enlargement of mediastinal and in contact goats (60 ± 2.00) and the infected (23.33 ± 1.53) which
bronchial lymph nodes. There were areas of congestion and haem- is sero-negative, at P < 0.0001 (Table 3).
orrhagic lesions on the mucosal surfaces of the rumen, abomasum
and large intestine. Moreover, there were necrotic areas in the 4. Discussion
small intestine. Localised petechial haemorrhages were observed
on the liver lobes and kidneys of dead animal. A marked inflamma- This recent outbreak of PPR in a small herd of goats in Ibadan
tion of the mesenteric lymph nodes was also noticed. has confirmed the presence of PPR in Nigeria and sub-Saharan

Please cite this article in press as: Balogun FA et al. Field evaluation and confirmation of acute peste des petits ruminant outbreak in a flock of West African
dwarf goats in Ibadan, Nigeria. Int J of Vet Sci Med (2017), https://doi.org/10.1016/j.ijvsm.2017.08.004
 F.A. Balogun et al. / International Journal of Veterinary Science and Medicine xxx (2017) xxx–xxx 5

Africa. It remains a major cause for concern and a problematic as in PPR infection (possibly due to disruption of the Na+-K+ pump),
issue that needs urgent attention because of its aftermath effects these substances are found at high levels in the serum; this is in
on food security, transboundary transmission and unquantifiable consonance with the findings of Sharma et al. [31]. It was however
economic losses, especially to small scale farmers [5]. All the epi- observed that, as the infection progressed from the 10th to 15th
demiological findings associated with this study and history of pre- day post infection, the haematological and serum biochemical
vious PPR outbreaks are known to have predisposed the WAD parameters became more significant, due to progression of infec-
goats to the PPR outbreak; this is in consonance with the submis- tion from acute stage to death or recovery [21]. All the aforemen-
sions of FAO and Baazizi et al. [2,6]. The mortality recorded for this tioned and previously discussed factors are presumptive and
PPR outbreak peaked (67% of total mortality recorded) between 6 tentative diagnosis for PPR infection. The detection of morbilli
and 8 days PE, which supports the results of Baron et al. [21], that virus specific antibodies in the sera of PPR infected WAD goats is
the severity of clinical signs generally peaks between 6 and 8 days indicative of recent PPR outbreak in Ibadan; this is also in line with
post infection and can continue for up to 14 days leading to death previous diagnostic procedures carried out by FAO and Saliki [2,8],
or recovery from infection. This study shows that PPR is associated to confirm outbreaks of PPR in different locations. It was further
with very high morbidity (96%) and mortality (60%), this may be confirmed through the percentage inhibition, that out of the three
due to the acute nature, pathogenesis, mode of spread of the infec- categories of WAD goats exposed to PPRV, the survivors of this
tion and the ability of the causative agent (morbilli virus) to cause infection have the highest antibody titres, which is in tandem with
immuno-suppression in infected WAD goats, through the reduc- the findings of Santhosh et al. [32]. Also, the in-contact WAD goats
tion of CD4+T cells; which is in line with previous studies [22– with no clinical signs of PPR presented a high level of antibody,
23]. This immuno-suppression is further corroborated by a signif- probably they were nursing a sub-clinical PPR infection; which is
icant drop in levels of total protein and globulin which is a precur- similar to the findings of Sen et al. [33] that exposed or in-
sor for immunoglobulins (antibodies) of the infected WAD goats contact cattle seroconverted and maintained PPR virus specific
[24]. This study shows that the WAD goats in the post exposure antibodies after day 21 post infection.
groups have higher values for WBC, when compared with the
pre-infection group; this is contrary to the leukopenia synonymous 5. Conclusions
with PPR outbreaks; which has been previously reported [25,26],
that within the 4–10 days PE to PPR, there is destruction of the PPR is a contagious infection that affects number of organs and
WBC and subsequent immuno-suppression [27]. The high values systems in small ruminants. The outcomes of this study will serve
for WBC could be attributed to the regeneration of damaged cells as a guide and template to subsequent research and diagnostic pro-
after the acute phase of the infection; and subsequently there were cedures in this field; and will contribute to the repository of
varying levels of antibodies, which is in line with a previous study knowledge. Regional vaccination of sheep and goats before the
[26], which concluded that the level of antibodies increased signif- age of 6 months is hereby recommended in endemic areas.
icantly after days 28–35 post infection with virulent PPR virus. On
the other hand, the low levels of RBCs, [Hb], PCV, MCV and MCH
compared with the control and normal physiological range of val- Competing interests
ues [18,19], could be attributed to the erosion, necrosis and con-
gestion associated with PPR, and also to the different phases of The authors declare no competing interests.
the disease, presence of secondary infections, nutritional status,
and/or level of dehydration [28,29]. There was a sharp drop in Acknowledgements
the blood glucose level, termed hypoglycaemia; this condition
occurs whenever there is a difficulty with the conversion of glyco- The authors of this study sincerely wish to appreciate the man-
gen to glucose (glycogenolysis). The liver is normally a principal agement and staff of Federal College of Animal Health and Produc-
store house for glycogen, but due to the functional impairment tion Technology, Moor Plantation, Ibadan; especially workers in
as a result of PPR infection, hence the short fall [2,8]. Liver damage, the student research farm and ruminant unit; and Prof. F.O. Fasina
as a result of PPR infection is further confirmed by an excessively (Country Team leader ECTAD, FAO-United Nations, Kenya).
high level of ALP and AST when compared with the control and
normal physiological values [18,20], these are serum enzymes References
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Please cite this article in press as: Balogun FA et al. Field evaluation and confirmation of acute peste des petits ruminant outbreak in a flock of West African
dwarf goats in Ibadan, Nigeria. Int J of Vet Sci Med (2017), https://doi.org/10.1016/j.ijvsm.2017.08.004