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DOI: 10.5281/zenodo.17541207
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Volume – II Issue- VI (No embe -Decembe ) 2025
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Su gical managemen o ail gang ene (Degnala) in bu alo: Case epo
R. Bas ako i1,2*, S. Upadhayaya3
1 Madi Ve e ina y Hosp al, Chi wan, Nepal
2 Ins i u e o T opical Medicine An we p, Belgium
3 Louisiana S a e Uni e si y, USA
| Recei ed: 15.10.2025 | Accep ed: 23.10.2025 | Published: 06.11.2025
*Co esponding au ho : R. Bas ako i
Madi Ve e ina y Hospi al, Madi, Chi wan, Nepal
INTRODUCTION
“Degnala” is an endemic, mos ly e al disease o bu alo ha
occu s in low, plain, and limi ed opog aphic a eas in wes e n Asia,
such as Nepal and India. Acco ding o Shi low (1939), Degnala
disease was named so due o he i s occu ence o his disease in
he a ea nea Deg Nala (Deg Ri e ), a ea o Pakis an in 1929-30.
Degnala is mo e p e alen in paddy g owing pa s in he mon h o
win e (Jada and Mis y, 1997). Poo quali y o paddy and whea
s aw in ec ed wi h Fusa ium ungus is belie ed o be he main
cause o degnala diseases. O e all malaise, edema o he
ex emi ies, gene al was ing wi h nec osis, and epide mal
sloughing a e all symp oms o his disease. In ec ions ha a e
debili a ing in na u e can esul in la ge economic losses due o
lowe p oduc ion, which is compounded by lowe g ow h a es,
dea h, and poo animal pe o mance.
MATERIALS AND METHODS
Case desc ip ion and his o y
A hi d pa i y emale bu alo was p esen ed o in Ve e ina y
Hospi al, Madi, Chi wan, Nepal in Augus , 2021 wi h a his o y o
in ec ion on he ail. Owne e ealed ha he bu alo was kep
Abs ac
Degnala is a ungal disease caused by Fusa ium species and is mo e p e alen in la ge uminan s. This case s udy was made o
unde s and he impo ance and e ec i e ea men o he disease. The hema ological in es iga ion e ealed ha he blood
pa ame e s we e no mal excep inc eases in numbe o RBC, Monocy es and eosinophil. The su gical app oach was done o
co ec he condi ion in which ail was ampu a e om he si e abo e he in ec ed egion o ail. Pos -su gical complica ions we e
none and eco e y was e y sa is ying.
Keywo ds: Tail Gang ene, su ge y, degnella
Copy igh © ISRG Publishe s. All igh s Rese ed.
DOI: 10.5281/zenodo.17541207
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unde s aw eeding and mos ly he animal was s alled ed. The
owne e ealed ha he s aw was a bi moldy as well and he body
condi ion o bu alo was good wi h no mal i als.
Clinical obse a ions
On clinical obse a ion, closely ind wi h he p inciple clinical sign
o swelling ail and hen d ying, nec osis and gang enous lesion
and sloughing o supe icial skin on ail. Examina ion e ealed ha
he e is no mal ec al empe a u e, hea a e, espi a ion a es,
capilla y e ill ime, pinkish mucous memb ane and no mal eeding
and wa e ing.
Su gical p ocedu e
Bu alo was kep unde epidu al anes hesia wi h 2% lignocaine
HCl a he junc ion o C1 and C2 while he animal was in s anding
posi ion. Du ing su gical p ocedu e, sepa a ion o subcu aneous
issue laye s, liga ion in e e y opening o blood essel was made
by ca gu 2-0. Excision o ail (Figu e 1) abo e he in ec ion was
done wi h an ellip ical incision on he skin so ha su u ing will be
easie . Tail below was emo ed comple ely and su u e o skin was
done wi h p olene No. 1 size (Figu e 2). A e comple e d essing
he su u e a ea is comple ely co e ed wi h ape (Figu e 3).
Figu e 1: In ec ed ail
Figu e 2: Su u ing o incised
a ea
Figu e 3: The su u e a ea is
comple ely co e ed wi h ape
Figu e 4: Remo ed segmen o
ail
Pos -ope a i e ca e
Animal was gi en meloxicam on nex day and cou se o an ibio ics
wi h amoxicillin and po assium cal una e was done o 3 days.
A e 15 days su u e is emo ed and was healing well. The e we e
no pos -ope a i e complica ions and bu alo was comple ely
eco e ed wi hin 15 days.
MAJOR FINDINGS
As shown in Table-1, he e we e no ema kable abno mali ies we e
ound wi h hema ological pa ame e s excep sligh inc ease in
RBC, Monocy e and Eosinophil.
Table 1. Shows he di e en hema ological and se ological pa ame e s
Hema ological
Pa ame e s
Findings
Re e ence alue
Se ological pa ame e s
Findings
Re e ence
alue
HB (gm/dl)
10.3
9-12
To al p o ein (gm/dl)
6.8
4.1-7.0
RBC*1012/l
8.6
5-7.3
Albumin
3.0
2.5-3.8
WBC*109/l
3.20
4-12
ALT (IU/L)
18
15-45
PCV%
34
30-36
AST(IU/L)
30
25-40
Neu ophil%
20
25-35
To al Bili ubin (mg/dl)
0.2
0.1-1.7
Monocy e%
8.6
3-7
BUN (mg/dl)
6.5
6-27
Eosinophil%
6.3
2-4
C ea inine (mg/dl)
0.95
0.91-2.0
Lymphocy es%
57.7
45-65
Alkaline phospha e (IU/L)
120
40-150
DISCUSSION
In he p esen case, he e ec ed pa o ail was excised and
emo ed ca e ully. Degnala was diagnosed on he basis o his o y
o eeding and obse a ion o a ec ed animal. Acco ding o Ka ki
(2012) myco oxin p oduced by he me abolism o Fusa iam ungus
cul i a ed on paddy/ ice s aw dissol es collagen and elas in in o
collagenase and elas inase, espec i ely, and is one o he leading
causes o Degnala disease. As a esul , blood low o he dependen
egions o he ea , ail, and oo is es ic ed, and issue e en ually
dies o anoxia. Feeding moldy ice s aw by animal in his case was
in line wi h Dandapa e al. (2011); Beh a, (1988); Kal a e al.
(1977). Expe imen al eeding o Fuso ium con aining s aw was
pe o med in bu aloes (Kal a, 1973; Beh a, 1988) and in bu alo
cal es wi h F. equise i (Kwa a, 1980) wi h F. oxyspo um
(Dandapa e al., 2011). Since occu ence o he disease has been
associa ed wi h he eeding o ice s aw, selenium oxici y is
suspec ed o play some ole, di ec ly o indi ec ly, in he
de elopmen o he disease (Bha ia & Gup a, 1986; Sha ma. 1984)
CONCLUSION
The p esen s udy e ealed ha he Degnala diseases was mos ly
ela ed and obse ed in animals eeding on ungal in ec ed s aw.
Typical clinical sign o he disease can be obse ed in he
ex emi ies and bes ea men is su gical emo al o a ec ed pa .
Du ing eeding ca e should be aken no o eed s aw in ec ed wi h
ungus.
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DOI: 10.5281/zenodo.17541207
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REFERENCES
1. Beh a G. D. (1988). Clinicopa hological s udies on
expe imen al Degnala disease in bu alo cal es. In:
P oceedings o II Wo ld Bu alo Cong ess. New Delhi:
ICAR (Indian Council o Ag icul u al Resea ch). (4)
103-108.
2. Bha ia KC, Gup a RK. (1986). Degnala disease and i s
di e en ial ea u es om selenium oxici y. Ha yana
Fa ming. 3:1-3
3. Dandapa , P., Nanda, P. K., Bandyopadhyay, S.,
Kaushal, A., & Sikda , A. (2011). P e alence o Deg
Nala disease in eas e n India and i s ep oduc ion in
bu aloes by eeding Fusa ium oxyspo um in es ed ice
s aw. Asian Paci ic Jou nal o T opical Medicine, 4(1),
54-57. h ps://doi.o g/10.1016/S1995-7645(11)60032-1
4. Jadha , K.M., Mis y, J.N. (1997). A clinical eco d o
spon aneous Deg Nala disease like disease in bu aloes in
semi a id Banaskan ha dis ic o Guju a s a e. Indian
jou nal o e e ina y esea ch., 6: 32-6
5. Kal a DS, Bha ia KC. (1990). Degnala disease in
bu aloes and ca le: epidemiological in es iga ions. J
En i on Pa hol Toxicol Oncol 1990; 10: 132-5
6. Keda Ka ki. (2012). Why Degnala disease epidemic in
bu aloes h oughou Sou h Eas Asia his yea ?
h p://en.engo mix.com/MA-
dai yca le/heal h/a icles/degnala-disease 2185/165-
p0.h m
7. Kwa a MS. (1980). Myco oxicosis as a possible cause o
gang enous synd ome in bu aloes - a p elimina y epo .
Indian J Anim Heal h; 19: 67-9.
8. Sha ma S. (1984). Selenium esea ch in India.
In e na ional Jou nal o En i onmen al S udy; 22: 231-
9. Shi low, J.E. (1939). Deg Nala disease o bu aloes: An
accoun o he lesions and essen ial pa hology. Indian
Ve e ina y Science and Animal Husband y. 9: 853-864.
