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Usman Talib.* and  Sami Ullah Khan Bahadur*

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Faculty of Veterinary Science, University of Agriculture, Faisalabad,



The official French name Peste des
petits ruminants (PPR) or ovine rinderpest is also known as kata,
pseudorinderpest, pneumoenteritis complex and stomatitis-pneumoenteritis
syndrome (A).The causative agent of
the disease is PPR virus (PPRV) which belongs to the genus Morbillivirus of the family Paramyxoviridae in the order Mononegavirales (International
Committee on Taxonomy of Viruses, 2012).These highly
contagious viruses include measles, canine distemper, rinderpest, peste des petits
ruminants, phocid distemper and cetacean morbillivirus (B). PPR is highly contagious disease of small ruminants caused by Peste
des petits ruminants virus (PPRV)
primarily infects sheep and goats (C). There is very close
relationship between PPR virus and Rinderpest virus (D).




The disease,
described firstly in West Africa in 1942 (E), was reported mostly in African countries (F, 9, 10, 11) and in
Middle East (G, 13),
South Asia (14, 15, H),
Central Asia (I)
and in the Arabic peninsula (18).
In Pakistan, PPR was reported for the first time in
1991 (j).


The disease can cause up to 100% morbidity and
90% mortality in a susceptible Population (K)


Levels of naturally or acquired immunity
mostly influences the wide range of reported values as well as differences
between species (sheep or goats) and production systems (L).
The virus exists as single serotype and four distinct lineages viz.,
I, II, III and IV have been reported (M). The virus is
able to enter lymphocytes and certain types of epithelial cells (N)

are three proteins associated with the host cell membrane –derived viral
envelope viz. matrix protein, fusion protein and HN protein. The pathogen is
sensitive to environmental changes and rapid inactivation occurs when exposed
to unfavorable conditions outside the host, therefore, close contact is
required for the virus to be transmitted from infected to susceptible animal O.


Initial replication
is at the lymph nodes draining the naso- and oro-pharynx, then there is viremia,
with virus entering epithelial cells of the intestine and lung. The intestinal
phase tends to be severe in younger animals, probably because of the slower
turnover rate of the enteric epithelium. The PPR virus enters and replicates in
both crypt and villus cells. Damage is especially severe in the parts of
intestine associated with lymphoid tissue because there is augmented viral
presence here.

At the same time
the virus is replicating in and damaging the intestine, it is also infecting cells
at the bronchiolo-alveolar junction, beginning a bronchointerstitial pneumonia.
So animals that survive the intestinal phase of the disease often succumb to a


Clinical finding, history.

A 2-year old buck of local
bread of Pakistan, teddy mix was presented to CMS, UAF with the history of
anorexia, coughing and diarrhea from 4 days,

On investigation owner told
about an other goat with same clinical sign died last day and also the 2 other
kids have diarrhea with no coughing and normal feeding.

Visually the buck wad
depressed with ocular discharge, slight nasal discharge, stomatitis with gum
and tongue necrosis and erosion, swollen pre-scapular lymph node and high temp
of 41oc was observed.

On auscultation, harsh
vesiculobronchial sound were heard.

Upon Fecal examination animal
was negative for parasitism.

CBC report revealed

Complete blood count (CBC) (Table. 1) as
an indicator of PPR virus infection (Rajak et al., 2005).

On the basis of history, clinical
sign, physical examination and CBC report the disease was diagnosed as PPR.



After confirming the disease
we treated the disease symptomatically because still there is no specific
treatment available for this disease.

Symptomatic and supportive treatment was
done because there is no specific treatment (http:// osp.mans. /
elsawalhy /Inf–Dis/PPR.htm).






gel (miconazole 20mg/g)






Case Management


The disease is
transmitted by direct and indirect contact PSick goats and sheep generate aerosols containing
infective droplets. Successful transmission therefore requires close contact
between sick and healthy animals. Fomites do not play a role in transmission of
the virus Q. Large amounts of the virus are
present in all body excretions and secretions, especially in diarrheic feces.
Infection is mainly by inhalation but could also occur through conjunctiva and
oral mucosa R.



Differential Diagnosis:

Mouth lesion –
rinder pest , FMD , Contagious ecthyma

Difficult breathing- pnenomian , CCPP

Diarrhea coccidiosis or gastrointestinal
helminth infestations

Blue tounge



In Pakistan, PPR is often diagnosed by
clinical signs and symptoms, postmortem examination and laboratory tests
including serological,culture and molecular techniques. In recent years various
molecular techniques including conventional PCR,real-time PCR has been used for
diagnosis of PPR { S }




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C . O zkul, A.,
Akca, Y., Alkan, F., Barrett, T., Karaoglu, T.,Dagalp, S.B., Anderson, J.,
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in goats. Comparative Immunology, Microbiology & Infectious Diseases 28:


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Obi, T.U., Taylor, W. and Diallo, A.: Recognizing peste des petit ruminants: a
field manual. Access
date, 2010.


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