PATHOG ENESIS of FMD
Virus particles first attach to mucosal epithelial cells, penetrate into the cytoplasm and replicate until the cells disintegrate.This releases more viral particles to infect other cells, including macrophages which drain into the efferent lymphatic system and then the blood.
Irrespective of the portal of entry, once infection gains access to the bloodstream, the virus is widely disseminated to many epidermal sites, probably in macrophages,
gross lesions develop only in areas subjected to mechanical trauma or unusual physiological conditions such as the epithelium of the mouth and feet, the dorsum of the snout of pigs and the teats.
Characteristic lesions develop at these sites after an incubation period of 1-21 d (usually 3-8 d in most species) .
The initial phase of viremia is often unnoticed and it is only when localization in the mouth and on the feet occurs that the animal is found to be clinically abnormal.
The experimental disease in sheep is characterized by an incubation period of 4-9 d after contact or 1-3 d after virus inoculation.
Thereafter, viremia occurs at 17-74 h and hyperthermia from the 17-96 h.
Clinical signs are serous nasal discharge, salivation and buccal lesions in 75% and foot lesions in 25 % of cases.
At the end of viremia, the animal recovers but the virus may persist in the pharyngeal area of convalescent ruminants as previously discussed.
Bacterial complications generally aggravate the lesions, particularly those of the feet and the teats, leading to severe lameness and mastitis, respectively.
In young animals, especially neonates, the virus frequently causes necrotizing myocarditis and this lesion may also be seen in adults infected with some strains of the virus, particularly type O.
CLINICAL FIN DINGS
In typical field cases in cattle, there is an incubation period of 3-6 d, but it may vary between 1 and 7 d.The onset is heralded by a precipitate fall in milk yield and a high fever (40-41"C; 104-106°F), accompanied by severe dejection and anorexia, followed by the appearance of an acute painful stomatitis.
At this stage, the temperature reaction is subsiding.
There is abundant salivation, the saliva hanging in long, ropy strings, a characteristic smacking of the lips, and the anirnal chews
carefully.
Vesicles and bullae (1-2 cm in diameter) appear on the buccal mucosa, dental pad and tongue.
These rupture within 24 h, leaving a raw painful surface which heals in about 1 week.
The vesicles are thin walled they rupture easily and contain a thin, straw-colored fluid.
Concurrently with oral lesions, vesicles appear on the feet, particularly in the clefts and on the coronet.
Rupture of vesicles causes acute discomfort and the animal is grossly lame, often recumbent, with a marked, painful swelling of the coronet.
Secondary bacterial invasion of foot lesions may interfere with healing and lead to severe involvement of the deep structures of the foot.
Vesicles may occur on the teats and when the teat orifice is involved, severe mastitis often follows.
Pregnant animals may abort or have stillbirths.
Very rapid loss of condition and fall in milk yield occur during the acute period and these signs are much more severe than would be anticipated from the extent of the lesions.
Eating is resumed in 2-3 d as lesions heal but the period of convalescence may be as long as 6 months.
Young animals are more susceptible and may suffer heavy mortality from myocardial damage, even when typical vesicular lesions are absent in mouth and feet.
In most outbreaks, the rate of spread is high and clinical signs are as described earlier but there is a great deal of variation in virulence and this may lead to difficulty in field diagnosis.
For example, there is a malignant form of the disease in adults in which acute myocardial failure occurs.
There is a typical course initially but a sudden relapse occurs on days 5-6 with dyspnea, a weak and irregular heart action, and death during convulsions.
Occasional cases show localization in the alimentary tract with dysentery or diarrhea, indicating the presence of enteritis.
Ascending posterior paralysis may also occur.
On the other hand, there is a mild form which usually occurs when endemic strains infect only indigenous Bos indicus (Zebu) cattle. 22. This is the form most commonly . seen in endemic countries in Africa, Asia and South America.
A sequel to FMD in cattle, due probably to endocrine damage, is
a chronic syndrome of dyspnea, anemia,
overgrowth of hair
and lack of heat tolerance.
Affected cattle are described colloquially as 'hairy panters'.
Diabetes mellitus has also been observed as a sequel in cattle.
CLIN ICAL PATHOLOGY
Identification of the agent in tissue or fluid.Virus isolation by inoculation into cell cultures or un weaned mice.
Immunological methods:
Enzyme-linked immunosorbent assay (ELISA)
Complement fixation test
polymerase chainreaction (RT-PCR)
Serological tests for specific antibody response to FMD
Virus neutra lization (VN),Solid-phase competitive enzymelinked immunosorbent assay (ELISA)
Experimental transmission.
The propagation of the virus in unweaned white mice can be used to detect the presence of virus in suspected material, the presence of antibodies in serum and for investigations into the transmission of immunity and the pathogenesis of the disease.In guinea pigs, intradermal injection of fresh vesicular fluid into the plantar pads causes vesicles to appear on the pads in 1-7 d and secondary vesicles in the mouth 1-2 d later.
CONTROL
(a) control by eradication and
(b) control by vaccination, or a combination of the two.