Clinical and Gross Pathological Findings of Johne's Disease in A Calf: A Case Report
Clinical and Gross Pathological Findings of Johne's Disease in A Calf: A Case Report
Clinical and Gross Pathological Findings of Johne's Disease in A Calf: A Case Report
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Clinical and gross pathological findings of Johne's disease in a calf: A case report
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Case Report
• Received: Aug 5, 2016 • Revised: Aug 19, 2016 • Accepted: Aug 20, 2016 • Published Online: Aug 20, 2016
AFFILIATIONS ABSTRACT
Faez Firdaus Abdullah Jesse Objective: This case report describes a clinical case of Johne’s disease (JD) in a
Muhammad Abubakar Sadiq Friesian calf calf aging one and half years.
Eric Lim Teik Chung Materials and methods: Physical examination of the calf was carried out, history
Idris Umar Hambali of the farm as well as samples for laboratory examinations were obtained. The
Abd Wahid Haron laboratory examinations included hematological examinations by direct wet
Department of Veterinary Clinical Studies, mount, hematocrit centrifugation technique and Giemsa stain, biochemical
Faculty of Veterinary Medicine, Universiti evaluation of serum, bacterial culture and isolation from feces and aspirate from
Putra Malaysia, 43400 Serdang, Selangor, the swollen jaw.
Malaysia. Results: Clinical history showed that the farm had a history of JD, and routine
health screening revealed that one of the calves had clinical signs suggestive of
Asinamai Athliamai Bitrus Johne’s disease. Physical examination of the calf revealed a lumpy jaw, enlarged
Yusuf Abba bilateral pre-scapular and pre-femoral lymph nodes, while hematological and
Mohd Azmi Mohd Lila biochemical findings showed a normocytic normochromic anemia, severe
Department of Veterinary Microbiology and leukocytosis with neutropilic left shift and lymphocytosis with hyperproteinemia
Pathology, Faculty of Veterinary Medicine, characterized by hyperglobulinemia. Fecal bacterial tests showed the presence of
Universiti Putra Malaysia, 43400 UPM acid fast bacilli. Based on the history and laboratory findings, the cow was
Serdang, Malaysia.
diagnosed with JD. In order to ensure effective control measures, the calf was
culled from the heard. Postmortem examination revealed inflamed pre-scapular
and pre-femoral lymph nodes with the presence of paraamphistomes in the
rumen mucosa.
Conclusion: Since JD is a chronic disease that lingers in livestock farms, there is
need for early identification and culling of infected animal in order to limit its
devastation on the farm.
CORRESPONDENCE KEYWORDS
Faez Firdaus Abdullah Jesse Acid fast, Bacilli, Calf, Gross pathology, Johne’s disease
Department of Veterinary Clinical Studies, Faculty of
Veterinary Medicine, Universiti Putra Malaysia,
43400 Serdang, Selangor, Malaysia.
E-mail: [email protected] How to cite: Jesse FFA, Bitrus AA, Yusuf Abba, Sadiq MA, Chung ELT, Hambali IU, Lila MAM,
Haron AW (2016). Clinical and gross pathological findings of Johne’s disease in a calf: A case report.
Journal of Advanced Veterinary and Animal Research, 3(3): 292-296.
http://bdvets.org/javar/ Jesse et al./ J. Adv. Vet. Anim. Res., 3(3): 292-296, September 2016 292
INTRODUCTION CLINICAL HISTORY
Johne’s disease (JD) is a chronic irreversible wasting A Friesian calf aging one and half years was presented to
gastro-enteric disease of ruminants caused by the University Veterinary Hospital (UVH), Universiti
Mycobacterium avium subsp. paratuberculosis (MAP) (Geraghty Putra Malaysia (UPM) with a complaint of weight loss.
et al., 2014). The disease was first reported in cattle in The farm had previous history of JD. Physical
1895 in Europe and 1908 in the United States (Sweeney examination of the calf showed the presence of lumpy
et al., 2012). The disease is mostly found in domestic jaw, enlarged bilateral pre-scapular and pre-femoral
ruminants such as cattle, buffaloes, sheep, goats and lymph nodes (Figure 1 and 2) and diarrhea. The mucus
camels. JD affects about 40% of dairy cattle worldwide. membrane was pink with a capillary refill time of 2 sec,
The infected cattle remain as carriers for years and shed while the body condition score was 2/5.
the organism via milk, colostrum and feces, and
subsequently contaminate feed and water (Facciuolo et
al., 2013). In addition, calves remain as asymptomatic
carriers for a period of 2 to 5 years. In Malaysia, JD has
been previously reported in a dairy farm in 2013
(Abdullah et al., 2013). However, sporadic cases JD have
also been reported in dairy farms in Malaysia.
Figure 1. Photograph of calf showing emaciation and Figure 4. Enlarged and hyperemic pre-femoral lymph
lumpy jaw (arrow). node (arrow).
Jesse et al./ J. Adv. Vet. Anim. Res., 3(3): 292-296, September 2016 293
disease difficult (Britton et al., 2015). The initial findings
of this case report showed that even though the calf had
a poor body condition score, it had a good appetite. This
is suggestive of a classical case of JD in ruminants. In
addition, clinical findings of lumpy jaw, enlarged bilateral
prescapular and prefemoral lymph node and diarrhea
were observed in this case. It is important to note that, at
the earliest stage of JD, lesions are confined to the lining
of the small intestines and the mesenteric lymph nodes.
The lesions later spread to the jejunum, ileum, caecum,
terminal end of the small intestine, colon and the
mesenteric lymph node as the disease progresses
(Sweeney et al., 2012). The manifestation of these gross
Figure 5. Rumen mucosa with paraamphistomes. lesions leads to malabsorption, protein leakage and
subsequently severe weight loss. In clinical cases of JD,
DIAGNOSTIC WORK UP AND RESULTS loss of proteins is reflected by lower protein and albumin
concentrations in the serum, without changes in globulin
concentration (Clarke, 1997). In advance cases, edema of
Whole blood was collected for hematology, direct wet
the submandibular and other dependent areas may be
mount, hematocrit centrifugation technique (HCT) and
seen (Clarke, 1997). In addition, rough and unthrifty hair
Giemsa stain. Serum was collected for biochemical
evaluation, while fluid aspirate from the swollen jaw as coat, alopecia and in some cases with pigmentation. This
was also reported in this case as the calf had lumpy jaw
well as fecal sample were collected for bacterial culture,
isolation and identification. Hematological and and unthrifty hair coat. However, in this case, there was
increased total protein associated with hyperglobulinemia.
biochemical findings showed normocytic normochromic
This may be associated with active antibody production
anemia, severe leukocytosis with neutrophilic left shift
by the immune system in the form of immunoglobulins
and lymphocytosis with hyperproteinemia characterized
to fight the infection.
by hyperglobulinemia (Table 1). Fecal culture revealed
the presence of an acid fast bacilli. There were no
In this case, the clinical history stated that the farm had a
bacterial growth from the fluid collected from the
swollen jaw. From the laboratory findings, clinical history of JD and it can be inferred that the calf might
examination findings and history of the farm, the calf was have be infected via contamination of feed with feces of
shedders or from the dam through colostrum (Sweeney,
diagnosed with JD.
1996; Pant et al. 2014; Robins et al., 2015).
POSTMORTEM EXAMINATION
The pathognomonic signs of MAP in cattle include
There was no therapeutic plan for this case, hence the chronic and intermittent diarrhea to progressive weight
calf was culled according to the guidelines described by loss from mild to severe, as was observed in this case
Mueller (2015) in order to reduce the spread of the (Clarke, 1997). This is consistent with the findings of this
disease in the herd. At postmortem examination, the case report, because the calf was looking cachetic and
carcass was emaciated and there was an absence of with a body condition score of 2/5 (Figure 1). Other
omental fat in the viscera. The pre-scapular and pre- clinical manifestation includes fall in milk yield in the
femoral lymph nodes were swollen and hyperemic absence of pyrexia and toxemia in cows (Abendaño et al.,
(Figure 3 and 4). The rumen was full with ingesta and 2013). In ruminant however, weight loss is as a result of
numerous para-amphistomes were seen attached to the malabsorption of protein and losses due to significant
rumen papillae (Figure 5). All other organs appeared to cellular infiltrate and edema that occur in the intestine
be apparently normal in size, consistency and texture. (Salem et al., 2013). The development of the onset of
clinical disease overwhelms the compensatory mecha-
DISCUSSION nisms of increased protein synthesis in the liver. The
above findings classically describe the condition of the
JD poses a significant economic and public health calf reported in this case.
implication to humans and the cattle industry (Gowozdz,
2008). This is due to the unavailability of accurate tests to The presence of E. coli and Bacillus cereus isolated from
diagnose different stages of the disease,which in turn fecal sample connotes theirs presence as normal floras of
makes the diagnosis, prevention and control of the the intestine, rather than the cause of the diarrhea as
Jesse et al./ J. Adv. Vet. Anim. Res., 3(3): 292-296, September 2016 294
Table 1. Results of laboratory investigation.
Parameters Animal identification
T1403 Reference values
RBC × 1012/L 5.65 5-10
Hb g/L 76.1 80-150
PCV L/L 0.25 0.24-0.46
WBC × 109/L 23.3 4.2-12
Band Neutrophils × 109/L 0.47 <0.2
Seg. Neutrophils × 109/L 6.99 0.6-4.0
Lymphocytes × 109/L 13.28 2.5-7.5
Total protein g/L 89.9 55-75
Albumin g/L 33.7 25-40
Globulin g/L 56.2 27-45
A:G 0.6 0.8-1.2
Direct wet mount - n/a
HCT - n/a
Giemsa stained blood film Theileria 0.1% n/a
Modified McMaster Strongyle 400 e.p.g n/a
Coccidia 300 o.p.g
Acid fast Bacteria + n/a
Hb=Hemoglobin, RBC= Red Blood Cell, PCV= Packed Cell Volume, WBC= White Blood Cells, A:G= Albumin-Globulin Ratio, n/a=not applicable
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