Salmon In Brine,Smoked Salmon Brine,Salmon Chunks In Brine,Sunflower Canned Salmon Tropical Food Manufacturing (Ningbo) Co., Ltd. , https://www.tropical-food.com
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Contact: MS. Sunny Wang
Product Description
Name
Canned Salmon
Flavor
Brine, Oil, Salad, Chili
Type
Shred, Flake, Chunk, Solid
Certificates
EU, FDA, BRC, HALAL,HACCP,KOSHER
Net weight
140g, 160g, 170g, 185g, 200g, 1kg, 1.88k.
Brand
Our brand or OEM, ODM
Shelf life
3/4 Years
MOQ
1X20'FCL
Payment terms
T/T, L/C
Delivery time
25 days after label artwork confirmed and advance payment done.
Packing
normal lid or easy open,paper label or lithio can, paper carton or shrinked by tray
EU NO.
3302/01034
RUSSIA NO.
3302/01034
Shipping docs
Commercial Invoice
Packing List
Bill of Lading
Certificate Of Origin/ Form A
Health Certificate
Veterinary Certificate
Catching certificate
Or as per customer`s request
Actinobacillus porcine
Diseases Overview Actinobacillus porcines can cause septicemia and death in pigs. There are also reports from individual pig-raising countries (Van Dorssen and Jaartsveld, 1962; Cutlip et al., 1972; Windsor, 1973; Mair et al., 1974; Mac Donald et al. 1976) pointed out that the incidence of suckling pigs and newly weaned piglets is related to Actinobacillus equisimilis. According to reports (Miniats et al., 1989), pigs and sows in swine outbreaks in Canada resembled swine erysipelas-like porcine actinomycosis; in the United States (Yaeger, 1996) and in the United Kingdom, porcine pneumonia-like pleurisy caused by the bacteria occurred in the United States (Yaeger, 1996) and the United Kingdom. disease. Most outbreaks have caused the sudden death of one or more piglets in the herd. Actinobacillus porcine infection may be widespread, but reports of the disease are rare. Pathogens Actinobacillus porcines are gram-negative, non-motile, non-decidua, aerobic or facultative anaerobic bacilli, lengths 0 to 5 μm, widths 0 to 8 μm. May appear filamentous. On blood agar, Actinobacillus porcines formed gray, viscous, round, translucent colonies with a diameter of 1 to 2 mm within 24 h. On horse blood agar, a narrow, but distinct, alpha-lysed blood zone appears around the colony; whereas on calf and sheep blood agar, there is a broad beta-total (complete) hemolytic zone. Grow on MacConkey agar. With biochemical methods, Actinobacillus porcinus and other related bacteria from pigs can be distinguished. Actinobacillus porcines can produce catalase, oxidase and urease; hydrolyzed esculin; can use aldose, lactose, water Yang glycosides and trehalose produce acid but do not produce gas, and do not utilize mannitol or sorbitol. Bada et al. (1996) recently studied their biochemical properties and antigenicity. Actinobacillus porcines and A. pleuropneumoniae? biotype II are indistinguishable, but biochemical methods and DNA analysis are available. Method for identification. The differences between Actinobacillus amaurosis and Actinobacillus porcinus: non-hemolytic, can use mannitol to produce acid, does not break down arabinose, cellobiose and salicin; it does not break esculin. Actinobacillus porcines has a pathogenicity in mice and A. catarrhalis does not. At 15 oC for 60 min, Actinobacillus porcellus and Actinobacillus equina can be killed, both of which are sensitive to disinfectants. A few days died on the medium and the disease. Epidemiology Actinobacillus porcinus has been isolated from the tonsils and nostrils of healthy pigs of all ages and the vagina of healthy sows (Ross et al., 1972). Neonatal piglets, piglets, and newly weaned pigs have a prevalent onset in the clinic, while sows and adult pigs rarely develop disease (Miniats et al., 1989; Sanford et al., 1990). Since pigs and horses are raised separately in modern farms, it seems that pigs are infected with A. cerevisiae. Clinical disease outbreaks caused by Actinobacillus porcines infection appear more frequently in less diseased and other highly healthy herds (Miniats et al., 1989; Sanford et al., 1990). This may be due to the lack of immunity of these pigs, allowing the virulent porcine actinomycete pathogens to fully exploit their pathogenic potential, but when the disease is no longer present, pathogens can be isolated from surface-healthy herds. Pathogenesis The pathogenesis of swine infection with Actinobacillus porcinus remains unclear. The infection appears to have occurred through the upper respiratory tract. It has been reported that the onset of disease caused by muscle vaccination (Fenwick et al., 1996) produces the same results as invasion through skin and mucosal lesions. In susceptible animals, the thrombus of spoilage can quickly spread to various organs and tissues throughout the body, forming embolisms in the blood vessels or adhering to the blood vessel walls. Forms microcolonies surrounded by hemorrhage and necrosis. The virulence factors of Actinobacillus porcinus have not yet been determined, but the lipopolysaccharides, cell wall polysaccharides, outer membrane proteins, and 104 kD hemolysin (?ApxI?) of some strains are potential virulence factors that appear to be involved in pathogenicity. . Anti-ApxI antibodies have been shown to be present in sera of experimentally infected convalescent pigs (Fenwick et al., 1996). Pigs die 15 h after infection. Clinical symptoms One or more piglets that die for 2 to 4 weeks suddenly die. This is usually a sign of brucellosis. Sometimes the death of the piglet provides the wrong judgment. Verticillium wilt, blood stasis, fever (to 40°C) and wheezing, sometimes accompanied by tremors and/or swaying, may be a sign of frequent piglet deaths and end-stage congestion (which can lead to necrosis of the feet, tail and ears) and Swollen joints. According to reports, piglets that have been weaned have anorexia, fever, persistent cough, shortness of breath (Yaeger, 1996) and pneumonia, and the growth of rehabilitation pigs is retarded. When the disease occurs in an adult animal, it is characterized by fever, round and diamond skin necrosis, loss of appetite and sudden death, but the mortality rate is usually low. It has been reported that sows have metritis, meningitis and miscarriage. The disease is easily confused with erysipelas, especially when skin necrosis occurs and respiratory symptoms are caused by pleuropneumonia. The most significant pathological changes in pathology are hemorrhagic pleuropneumonia caused by bleeding in the lungs, kidneys, heart, liver, spleen, skin, and intestines. The most common site of lesions was the lungs, which showed necrosis of lung lobule and fibrin exudation. Visible increase in plasma and fibrin exudates in the chest and pericardium. Lungs, liver, skin, mesenteric lymph nodes, and kidneys of older piglets and weaned piglets have pleurisy, pericarditis, and miliary abscesses. Pulmonary lesions are signs of pleuropneumonia, and arthritis (Van Dorssen and Jaartsveld, 1962; Odin, 1994) and valvular inflammation (Jones and Simmons, 1971) have also been reported. In adult animals, a large number of round, rhomboid or irregularly shaped skin lesions usually appear. Histopathological examination revealed that bacterial plugs accompanied by hemorrhagic necrosis of fibrin were attached to the blood vessels of the lung, liver, kidney, skin, spleen, heart, pericardium, medullary membrane, and brain (Fig. 44.4). Bacterial embolism is surrounded by plum-like radial phagocytic leukocytes, which are most pronounced in the lungs and may have larger areas of necrotic foci fusion. The sudden death of individual piglets in a herd that has been diagnosed with Actinobacillus porcine disease usually indicates a new outbreak. Bleeding and necrosis of the lungs and/or skin and swelling of the kidneys and spleen indicate infection of Actinobacillus porcines. In the case of adult pigs with fever, loss of appetite, and erythroid lesions of the skin (especially when erysipelas have been immunized), A. porcines disease should be suspected. Microscopic lesions consisting of bacterial plugs, necrotic and inflammatory cells can also be seen in the lungs and other organs. Of course, the diagnosis needs to be separated from the lesion to Actinobacillus porcinus or Actinobacillus equina. When pleuropneumonia is suspected in a herd-free herd, Actinobacillus infection should be considered. In these herds, mild or atypical lung lesions and anti-ApxI antibodies are raised, but there are no A. pleuropneumoniae cytotoxins or their bacterial antigens (Fenwick et al., 1996). Actinobacillus porcineus can often be isolated from the tonsils of 2 to 10 days old piglets of this herd. Treatments Actinobacillus porcines are sensitive to most commonly used antibiotics. Because suckling pigs have a fast onset and no aura, they often have no time to take treatment. Adult pigs may be given orally or parenterally with ampicillin (5 mg/kg), intramuscularly with benzathine (promethazine), procaine penicillin G (2,25 - 3,010,6 IU), intramuscularly. Procaine penicillin (18 to 2?410?6 IU), or oxytetracycline hydrochloride hydroxide (550 g/t) and/or streptomycin added to the diet. The course of treatment for 1 week will be very good. Efficacy. Prevention Although these bacterins have not yet been rigorously evaluated, they have been used in swine with Acinetobacter porcine disease and have been shown to be successful.