2. NEWCASTLE DISEASE
NEWCASTLE CAUSATIVE AGENT
• Family: Paramyxoviridae
• Genus: Avulavirus,
• Species: Avian avulavirus 1.
• Type of nucleic acid: RNA
TRANSMISSION
Direct transmission occurs by exposure to fecal and other excretions
from infected birds.
3. Transmission
Indirect transmission through contact with contaminated food, water,
equipment, and clothing.
NDV is transmitted through infected birds' droppings and secretions from the
nose, mouth, and eyes. NDV spreads rapidly among birds kept in confinement,
such as commercially raised chickens.
Hatching chicks may be infected through egg for some NDV strains;
transmission of highly virulent isolates is uncommon.
PATHOGENESIS: The incubation period for the disease ranges from 4 to 6
days.
pathogenesis of Newcastle disease is based on the extensive necrosis of
lymphoid areas in the spleen and intestine mainly
4. Pathogenesis of NDV
• An infected bird may exhibit several signs, including respiratory signs (gasping,
coughing)
• nervous signs (depression, muscular tremors, drooping wings, twisting of head
and neck, circling, complete paralysis)
• swelling of the tissues around the eyes and neck, greenish, watery diarrhea.
ND strains are classified as lentogenic (lowly virulent), mesogenic (moderately
virulent) or velogenic (highly virulent) depending on the speed with which they
kill chickens or embryonated eggs.
They are also classified according to the predilection sites for virus infection as
pneumotropic (respiratory), viscerotropic (gastro-intestinal), or neurotropic
(nervous) strains.
5. a. Eyelid( lymphoid
hemorrhages)
b. Cecal tonsil(focal
hemorrhage and
necrosis)
c. Proventriculus(
multifocal
hemorrhages)
d. Spleen : multifocal
necrosis
6. GROSS LESIONS of NDV
1. Edema of the interstitial tissues of the neck
2. Hemorrhages and necrosis in the proventriculus, gizzard
and small intestinal wall.
3. Acute laryngitis and tracheitis congestion and catarrhal
exudates air sacs thickened and cloudy.
Psittacines and other birds can be reservoirs of infection and
can continue to excrete virus for up to 12 months after
recovering from clinical disease.
7. (A)Typical conjunctivitis
(B) Postmortem examination
showing hemorrhages of
intestine
(C)Enlarged spleen and
hemorrhages in mucosa
of proventriculus, along
with normal organs for
comparison.
8. MICROSCOPIC LESIONS of NDV
The histopathological lesion assessment was done
descriptively according to:
1. there is detection of viral nucleic acid mostly in
macrophages associated with lymphoid tissues.
2. There is lymphocyte depletion in splenic lymphoid follicles
so, they tend to completely disappear as the days go by
3. inflammatory cell infiltration in proventriculus lymphoid
tissues.
The severity of each organ was graded with the following
criteria: Focal lesion distribution (low severity), multifocal
(moderate severity), and diffuse (high severity).
9. CANINE PARVOVIRUS
• The canine parvovirus (CPV) infection is a highly contagious viral
illness that affects dogs.
• Family: Parvoviridae
• Genus: protoparvovirus. DNA naked
• Specie: canine parvovirus 2
TRANSMISSION: CPV is spread directly and indirectly by anything
contaminated by fecal material (shoes, coats, hands, equipment).
10. PATHOGENESIS of CPV
Once a dog or puppy is infected, there is an incubation period of three to seven
days before the onset of first symptom
Disease develop into two forms:
• Enteric form the virus usually begins by attacking the tonsils or lymph nodes
of the throat for one or two days, causing lymphopenia.
• Once in the bloodstream targets the bone marrow and in the cells that line
the walls of the small intestine does its worst damage epithelium the lining
the virus invades these crypts where new epithelial cells are born.
• Myocardial form In very young dogs, CPV can also infect the heart, leading to
inflammation of heart muscle, poor function, and arrhythmias.
• The heart form is associated with congestive heart failure. There is slower
onset of clinical signs: Dyspnea, Depression, Cough, Ascites, Death typically at
12–16 weeks of age
11.
12. Gross lesions of Canine
parvovirus
In the enteric form the following are seen:
• Lower and middle small intestine is dilated — contents are watery
Catarrhal enteritis ultrasound may reveal enlarged lymph nodes in the
groin
• Bone marrow is depleted
• thymic atrophy; and, in the case of CPV myocarditis, pale streaks in
the myocardium.
14. Microscopic lesions of CPV
• characterized by multifocal necrosis of the crypt epithelium and loss
of crypt architecture.
• Depletion of lymphoid tissue and cortical lymphocytes (Peyer's
patches, peripheral lymph nodes, mesenteric lymph nodes, thymus,
spleen)
• bone marrow hypoplasia
15. HEART-WATER (COWDRIOSIS)
• AETIOLOGY: Cowdriosis is a ricketsial disease of Ruminants caused
by Cowdria(Ehrlichia) ruminantium.
• a small, Gram negative, pleomorphic coccus
• Family: Anaplasmataceae and
• order: Rickettsioses.
• This organism is an obligate intracellular parasite.
• Transmitted by ticks of the genus Ambylomma variegatum
16. Transmission of heart water
• Heart water is transmitted by ticks of the genus Ambylomma.
• In ticks the transmission is trans-stadial or trans-ovarian. Infected
animals that recovered can be become chronic carriers for up to 8
months. The disease is not contagious.
• E. ruminantium affects cattle, sheep, goats and water buffalo.
• It can also infect some wild ungulates
17. Pathogenesis of heart water
• E ruminantium in the tick enter the host’s skin through the saliva
when biting the organisms may replicate first within the regional
lymph nodes then disseminate via the bloodstream to invade
endothelial cells of blood vessels elsewhere in the body
• Signs and lesions are associated with functional injury to the vascular
endothelium, resulting in increased vascular permeability without
recognizable histopathologic or even ultrastructural pathology.
• The concomitant fluid effusion into tissues and body cavities
precipitates a fall in arterial pressure and general circulatory failure.
18. Pathogenesis of heart water cont’d
• The amount of effusion seen, particularly in body cavities, is not
necessarily proportionate to the concentration of parasitic colonies
detected in endothelial cells.
• The lesions in peracute and acute cases are hydrothorax,
hydropericardium,
• edema and congestion of the lungs and brain, splenomegaly,
Petechiae and ecchymosis on mucosal and serosal surfaces, and
occasionally hemorrhage into the GI tract, particularly the
abomasum.
19. Macroscopic lesions
• lesions are hydropericardium,
hydrothorax, pulmonary edema,
intestinal congestion,
• Edema of the mediastinal and bronchial
lymph nodes, Petechiae on the
epicardium and endocardium,
• congestion of the brain, and moderate
splenomegaly.
22. Reference
• Heart water, In Veterinary Medicine, Saunders, 8th Ed, 1997, London
p. 1153-1155
• Newcastle Disease, In Merck Veterinary Manual, National Publishing
Inc. 8th Ed, 1998, Philadelphia, p 1941-1942.
• http://www.cfsph.iastate.edu/FastFacts/pdfs/heartwater_F.pdf
• Parvovirose du chien, In Dictionnaire Pratique de Thérapeutique
Canine et Féline, Masson, Forth ed, 1997, Paris, p 401-402
