PPR (Pestis des Petitis ruminants) IN SHEEP & GOAT

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PPR (Pestis des Petitis ruminants) IN SHEEP & GOAT
PPR (Pestis des Petitis ruminants) IN SHEEP & GOAT

PPR (Pestis des Petitis ruminants) IN SHEEP & GOAT

BY- Dr.Ajeet  Singh ,Veterinary surgeon,

Global Veterinary Clinic and Surgery Centre, Gorakhpur
PPR is stand for Pestis des pestitis ruminants. is a contagious disease affecting goats and sheep in Africa (from the Tropic of Cancer to the Equator), the Middle East and the Indian subcontinent.But since June 2008, the disease invaded Morocco, which indicates a crossing of the natural barrier of the Sahara. It is caused by a species of the Morbillivirus genus of viruses. The Disease is highly contagious, and has roughly an 80 percent mortality rate in acute cases.Recently the animal husbandry department of Govt. of India through its state AHD , has started the elimination programme of this disease . In that context , mass vaccination against ppr are being done in the rural and urban areas among goat and sheep.It is the most dreadful disease of sheep and goat. In India , it accounts approx 90% mortality hence it has much effect on the rural economy of India .
Others names of PPR:
It is also called as Ovine rinderpest , Goat plague, Pseudo Rinderpest, pest of small Ruminants and also called as KATA. Acute and Subacute viral disease of small ruminants that is characterized by fever, erosive stomatitis, conjunctivitis, gastroentritis and pneumonia.
Etiology of PPR:
The causative agent of PPR is belongs to family Paramyxovaridae genus Morbilli virus. This virus is antigenically related with the Rinderpest virus , canine distemper virus and human measles virus.
Epidemiology of PPR:
• PPR comes under the heading of list A diseases by OIE.
• Goats are more susceptible than sheep , mostly outbreaks are seen in Africa and Asia.
• Morbidity rate is 90%
• Mortality rate is 50-80%
• Directly (through infected animal ) and indirectly ( through Saliva, bedding material, feces ) disease is transmitted.
Pathogenesis of PPR:
After inhalation virus enters into the body cavity and reach the pharyngeal and submandibular lymph nodes where it starts multiply, after multiplication the virus enters into the blood and cause viremia within the three days of onset of infection. From here virus moves to lymphoid tissues that may lead to leuckopenia and immunosuppression and virus moves mucosa of GIT and respiratory tract. It cause gastroentritis and pneumonia.After it body temperature return to normal.
Clinical Findings of PPR:
• The incubation period of PPR is from 2-9 days.
• PPR Effected animal shows high rise of body temperature ranges from 105-106F.
• animal become dull, depressed ,anorectic and mucosal erosions in the passage of mouth and nasal cavity become evident within 5 days.This may lead to profuse salivation and necrotic stomatitis with halitosis.
• Later on nasal discharge becomes mucopurulent , severe respiratory distress is present that may lead to trachitis and pneumonia.
• signs of conjunctivitis.
• after 3 days of infection profuse watery diarrhea noted that may lead to dehydration , hypothermia and animal lead to death.
• Pregnant animals died because of high body temperature.
Post Mortem lesions of PPR :
• Necrosis , erosion’s , congestion , hemorrhages are present in the mouth and respiratory tract.
• zebra stripping is present in Colon is important sign of PPR.
• haemorrhagic gall bladder.
• Swollen and enlarged lymph nodes.
• White foci are present in pair patches.
Diagnosis of PPR :
• on this basis of history,clinical signs,Post-mortem lesions and Haematology
Treatment of PPR :
• No specific Treatment. Symptomatic and supportive drugs are given, Must keeps the antibiotic ( Tylosine) because mycoplasmosis and PPR occur in same season. due to rise in temperature NSAID is also given. Avoid use of steroids.
• If animal dull and depressed Dextrose .
• Immune boosters.
• dont waste money on anti diarrhea drugs.
• Indigenous medicine made of cocktail by mixing alum 50gm (powder) + pot. Permanganate 5gm. + Livertonic -50ml + multivitamins -50ml.+ haldi powder 50 gm. , make this cocktail paste in boiled brinjal, feed this cocktail morning and evening with rice gruel for 7days.
• It has very marvelous result.
Clinical signs
Clinical signs appear an average of two to six days after natural infection with the virus (the incubation period). This is followed by the sudden onset of fever with rectal temperature of at least 40° to 41oC. Affected animals are markedly depressed and appear sleepy. Their hair stands erect giving them a bloated appearance, especially the short-haired breeds. Soon after this stage, a clear watery discharge starts to issue from the eyes, nose and mouth, later becoming thick and yellow as a result of secondary bacterial infection . The discharges wet the chin and the hair below the eye; they tend to dry, causing matting together of the eyelids, obstruction of the nose and difficulty in breathing.
One to two days after fever has set in, the mucous membranes of the mouth and eyes become very reddened . Then epithelial necrosis causes small pin-point greyish areas to appear on the gums, dental pad, palate, lips, inner aspects of the cheeks and upper surface of the tongue. These areas increase in number and size and join together. The lining of the mouth is changed in appearance. It becomes pale and coated with dying cells and, in some cases, the normal membrane may be completely obscured by a thick cheesy material . Underneath the dead surface cells there are shallow erosions. In mild cases these changes may not be severe and will require careful examination to be seen. Gentle rubbing across the gum and palate with a finger may yield a foul-smelling material containing shreds of epithelial tissue. Similar changes may also be seen in the mucous membranes of the nose, the vulva and the vagina. The lips tend to swell and crack and become covered with scabs .
As the disease progresses, a characteristic foul smell exudes from the mouth. Affected animals resist attempts to open their mouths because of the pain.
Diarrhoea commonly appears about two to three days after the onset of fever ) although, in early or mild cases, it may not be obvious. The faeces are initially soft and then watery, foul-smelling and may contain blood streaks and pieces of dead gut tissue. Where diarrhoea is not an obvious presenting sign, the insertion of a cotton wool swab into the rectum may reveal evidence of soft faeces which may be stained with blood.
Affected animals breathe fast, sometimes so fast that they exhibit rocking movements with both the chest and abdominal walls moving as the animal breathes. Severely affected cases show difficult and noisy breathing marked by extension of the head and neck, dilation of the nostrils, protrusion of the tongue and soft painful coughs – they have obvious signs of pneumonia.
Such victims may eventually become dehydrated with sunken eyeballs, and death often follows within seven to ten days from onset of the clinical reaction. Other animals will recover after a protracted convalescence.
A common feature in later stages of the disease is the formation of small nodular lesions in the skin on the outside of the lips around the muzzle. The exact cause of these is not known (possibly Dermatophilus infection or reactivation of a latent contagious ecthyma infection – orf or “sore mouth”) but they cause confusion because of their similarity to the symptoms of primary contagious ecthyma or even sheep/goat pox.
Up to 100 percent of the animals in a flock may be affected in a PPR outbreak with between 20 and 90 percent dying. These proportions are usually lower in endemic areas where older animals have survived earlier infection. Pregnant animals may abort.
In summary, suspect PPR if you see any combination of:
• the sudden onset of a febrile illness affecting sheep and/or goats; eye, nose and mouth discharges with sores in the mouth, with or without scabs or nodules around the mouth;
• pneumonia;
• a significant death rate.
Any appearance of one or more of these signs in combination must be considered suspicious.
Post mortem findings
The carcass of an affected animal is usually emaciated, the hindquarters soiled with soft/watery faeces and the eyeballs sunken. The eyes and nose contain dried-up discharges. The following changes may be seen:
Mouth
Dirty-white, false membranes; erosions on the gums, soft and hard palates, tongue and cheeks and into the oesophagus.
Lips
Swollen; erosions and possibly scabs or nodules in late cases.
Nasal cavity
Congested (reddened) lining; clear or creamy yellow exudates; erosions.
Lungs
Dark red or purple areas; firm to the touch, mainly in the anterior and cardiac lobes (evidence of pneumonia) .
Lymph nodes (associated with the lungs and the intestines)
Soft and swollen. Abomasum Congested (reddened) lining; haemorrhages.
Small intestines
Congested (reddened) lining; haemorrhages; some erosions.
Large intestines (caecum, colon and rectum)
Small red haemorrhages along the folds of the lining, joining together as time passes and becoming darker, even green/black in stale carcasses
Differential diagnosis
PPR is frequently confused with other diseases that present fever and grossly similar clinical signs, especially when it is newly introduced. When carrying out an investigation, examination of the way the disease behaves in the herd or flock is as important as the findings on a single goat or sheep. The most frequent sources of confusion are:
Mouth lesions
Could be a symptom of: rinderpest, foot-and-mouth disease, bluetongue or contagious ecthyma (orf or “sore mouth”).
Difficult breathing
Could be a symptom of: pneumonic pasteurellosis or contagious caprine pleuropneumonia (CCPP).
Diarrhoea
Could be a symptom of: coccidiosis or gastro-intestinal helminth infestations. Pneumonia is usually a very obvious presenting sign in PPR so, without doubt, pneumonic pasteurellosis and CCPP have caused the most difficulty in differential diagnosis.
Pneumonic pasteurellosis
is a purely respiratory disease of sheep and goats caused by the bacterium Pasteurella haemolytica. Dark red/purple areas, firm to the touch, are evident mainly in the anterior and cardiac lobes of the lung . There are no oral lesions or diarrhoea. The numbers of affected and dead animals are usually lower than for PPR except under exceptional conditions of stress and crowding such as can occur when large numbers of sheep are assembled for trade. The main problem of differentiation arises when oral lesions and diarrhoea are either absent or not very obvious in PPR, as is sometimes the case. Using appropriate culture media, Pasteurella haemolytica bacteria are easily isolated in pure and profuse culture from pneumonic lungs of sheep, even from the lungs of PPR-affected animals. Isolation of Pasteurella haemolytica bacteria from the lungs of sheep, therefore, neither confirms a diagnosis of primary pneumonic pasteurellosis nor rules out the presence of PPR. Diagnostic tests for detecting PPRV should be carried out in all suspected cases of pneumonic pasteurellosis where there is a risk of PPR.
Contagious caprine pleuropneumonia (CCPP)
is a disease of goats (sheep are not affected) caused by a Mycoplasma sp. Like PPR, it is characterized by fever, difficult/abnormal breathing and coughing, but there mouth lesions or diarrhoea are not present in CCPP. At post mortem examination, the lung lesions in CCPP are more diffuse and a fibrinous fluid is found in the chest cavity. Fibrin deposits cover the lungs and are frequently connected to the chest wall by fibrinous strands . In PPR high-risk areas it is advisable to rule out PPR by laboratory testing of, at least, serum samples from convalescent flocks, even if CCPP is suspected.
Rinderpest disease
in small ruminants has been described primarily in Asia. Generally, this disease occurs in small ruminants only when they are in contact with affected cattle or buffaloes, so it is important during investigations to examine all species. Confirmation requires the resources of a specialist laboratory (see Sources of assistance). The samples required for laboratory confirmation of both rinderpest and PPR are identical. As the Global Rinderpest Eradication Programme (GREP) progresses, it becomes increasingly important that PPR and rinderpest be differentiated because, at this stage of the programme, any outbreak of rinderpest anywhere represents an international emergency.
Foot-and-mouth disease (FMD)
is more commonly seen in sheep than goats. The most important distinguishing features of FMD, other than the appearance of the lesions, are the absence of breathing problems and diarrhoea, and the presence of lameness (often marked). Sudden death of very young lambs without other signs often occurs. The oral lesions when present are often very small and difficult to see; the mouth does not exude such a foul odour as in PPR. Bluetongue, like PPR, is characterized by fever, discharges and oral lesions. However, it differs from PPR in: the presence of oedema of the head region; bluish discoloration of the oral cavity, the coronary band of the hooves and the less hairy parts of the body; and lameness.
Bluetongue
virus infection is endemic throughout the regions of the world affected by PPR. Clinical disease is, however, not generally experienced in indigenous breeds in these countries, being mainly restricted to exotic introduced animals. The presence of antibody to bluetongue viruses in single samples does not confirm a provisional diagnosis of bluetongue.
Contagious ecthyma (orf, “sore mouth”, contagious pustular dermatitis)
is often confused with PPR because of the nodules and thick scabs sometimes seen on the lips in the late stages of PPR. Confusion is especially likely to arise in severe cases of orf where lesions extend into the mouth and nose. In uncomplicated orf, there is usually no oral necrosis, diarrhoea or pneumonia.
Control of PPR
• Control of PPR outbreaks relies on movement control (quarantine) combined with the use of focused (“ring”) vaccination and prophylactic immunization in high-risk populations.
Reference-on request
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