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Vaccine /Animal Vaccine Overviews 

A vaccine is a biological preparation that provides active acquired immunity to a particular disease.
A vaccine typically contains an agent that resembles a disease-causing microorganism and is often made from weakened or killed forms of the microbe, its toxins or one of its surface proteins.
The agent stimulates the body's immune system to recognize the agent as a threat, destroy it, and keep a record of it so that the immune system can more easily recognize and destroy any of these microorganisms that it later encounters.
Vaccines can be prophylactic (example: to prevent or ameliorate the effects of a future infection by any natural or "wild" pathogen), or therapeutic (e.g., vaccines against cancer are being investigated).

The administration of vaccines is called vaccination.
The effectiveness of vaccination has been widely studied and verified; for example, the 
influenza vaccine
,[1] the HPV vaccine,[2] and the chicken pox vaccine.[3] 
Vaccination is the most effective method of preventing infectious diseases;
[4]widespread immunity due to vaccination is largely responsible for the worldwide eradication of smallpox and the restriction of diseases such as polio, measles, and tetanus from much of the world. The World Health Organization (WHO) reports that licensed vaccines are currently available to prevent or contribute to the prevention and control of twenty-five infections.[5]

The terms vaccine and vaccination are derived from Variolae vaccinae (smallpox of the cow), the term devised by Edward Jenner to denote cowpox. He used it in 1798 in the long title of his Inquiry into the...Variolae vaccinae...known...[as]...the Cow Pox, in which he described the protective effect of cowpox against smallpox.[6] In 1881, to honor Jenner, Louis Pasteur proposed that the terms should be extended to cover the new protective inoculations then being developed.[7]

The Strange History of Vaccines
(The Strange History of Vaccines—And Why People Fear Them)

Before vaccines, millions of children died horrific deaths each year from infectious diseases like whooping cough, polio, and measles. Today, thanks to vaccines, most of these diseases have been eradicated. Yet people in different corners of the world are rejecting vaccines. In the United States, more and more parents are refusing to have their children vaccinated because they believe a debunked theory that vaccines cause autism. Meanwhile, in Pakistan and Afghanistan, health workers are regularly targeted because vaccines are thought to be a Western plot .....

List of epidemics
This article is a list of epidemics of infectious disease. Widespread and chronic complaints such as heart disease and allergyare not included if they are not thought to be infectious.

Smallpox is believed to have been acquired by humans originally as a zoonosis from a terrestrial African rodent between 16,000 and 68,000 years ago, well before the dawn of agriculture and civilization. The earliest physical evidence of it is probably the pustular rash on the mummified body of Pharaoh Ramses V of Egypt.[9] 

The disease killed an estimated 400,000 Europeans annually during the closing years of the 18th century (including five reigning monarchs),[10] and was responsible for a third of all blindness.[6]
Of all those infected, 20–60 percent—and over 80 percent of infected children—died from the disease.

Smallpox was responsible for an estimated 300–500 million deaths during the 20th century.[13][14][15] As recently as 1967, the World Health Organization (WHO) estimated that 15 million people contracted the disease and that two million died in that year.[5]

After vaccination campaigns throughout the 19th and 20th centuries, the WHO certified the global eradication of smallpox in 1979.[5] Smallpox is one of two infectious diseases to have been eradicated, the other being rinderpest, which was declared eradicated in 2011.[16][17][18]

Veterinary medicine

Vaccinations of animals are used both to prevent their contracting diseases and to prevent transmission of disease to humans.[82] Both animals kept as pets and animals raised as livestock are routinely vaccinated. In some instances, wild populations may be vaccinated. This is sometimes accomplished with vaccine-laced food spread in a disease-prone area and has been used to attempt to control rabies in raccoons.

Where rabies occurs, rabies vaccination of dogs may be required by law. Other canine vaccines include canine distemper, canine parvovirus, infectious canine hepatitis, adenovirus-2, leptospirosis, bordatella, canine parainfluenza virus, and Lyme disease, among others.

Cases of veterinary vaccines used in humans have been documented, whether intentional or accidental, with some cases of resultant illness, most notably with brucellosis.[83] However, the reporting of such cases is rare and very little has been studied about the safety and results of such practices. With the advent of aerosol vaccination in veterinary clinics for companion animals, human exposure to pathogens that are not naturally carried in humans, such as Bordetella bronchiseptica, has likely increased in recent years.[83] In some cases, most notably rabies, the parallel veterinary vaccine against a pathogen may be as much as orders of magnitude more economical than the human one.

Animal Vaccine Overviews

Avian reoviruses
Newcastle disease
Infectious bursal disease 傳染性囊腫疾病
Influenza A virus H5N6 subtype
Japanese encephalitis
Classical swine fever
Bovine ephemeral fever 牛暫時熱
Bovine herpesvirus 1
Infectious bovine rhinotracheitis
Avian reoviruses 禽呼腸孤病毒
Avian reoviruses belong to the genus Orthoreovirus, and Reoviridae family. They are non-enveloped viruses that undergo replication in the cytoplasm of infected cells. It has icosahedral symmetry and contains a double-shelled arrangement of surface protein. Virus particles can range between 70–80 nm. Morphologically, the virus is a double stranded RNA virus that is composed of ten segments. The genome and proteins that are encoded by the genome can be separated into three different sizes ranging from small, medium, or large. Of the eleven proteins that are encoded for by the genome, two are nonstructural, while the remaining nine are structural.[1]

Newcastle disease 新城疫病

Newcastle disease is a contagious bird disease affecting many domestic and wild avian species; it is transmissible to humans.[1] It was first identified in Java, Indonesia, in 1926, and in 1927, in Newcastle-upon-Tyne, England (whence it got its name). However, it may have been prevalent as early as 1898, when a disease wiped out all the domestic fowl in northwest Scotland.[2] Its effects are most notable in domestic poultry due to their high susceptibility and the potential for severe impacts of an epizootic on the poultry industries. It is endemic to many countries.

Exposure of humans to infected birds (for example in poultry processing plants) can cause mild conjunctivitis and influenza-like symptoms, but the Newcastle disease virus (NDV) otherwise poses no hazard to human health. Interest in the use of NDV as an anticancer agent has arisen from the ability of NDV to selectively kill human tumour cells with limited toxicity to normal cells.

No treatment for NDV exists, but the use of prophylactic vaccines[3] and sanitary measuresreduces the likelihood of outbreaks.

Infectious bursal disease 傳染性囊腫疾病
Infectious bursal disease (also known as IBD, Gumboro Disease, Infectious Bursitis and Infectious Avian Nephrosis) is a highly contagious disease of young chickens caused by infectious bursal disease virus (IBDV),[1]characterized by immunosuppression and
mortality generally at 3 to 6 weeks of age. The disease was first discovered in 
Gumboro, Delaware in 1962. It is economically important to the poultry industry worldwide due to increased susceptibility to other diseases and negative interference with effective vaccination. In recent years, very virulent strains of IBDV (vvIBDV), causing severe mortality in chicken, have emerged in Europe, Latin America, South-East Asia, Africa and the Middle East. Infection is via the oro-fecal route, with affected bird excreting high levels of the virus for approximately 2 weeks after infection.

Influenza A virus H5N6 subtype A型流感病毒的H5N6亞型
H5N6 is a subtype of the species Influenza A virus (sometimes called bird flu virus). Four known cases, three fatal, have occurred in humans as of July 12, 2015.[1][2][3][4]
2016[edit] In 2016 cases of H5N6 were reported alongside H5N8, and H7N9 across the globe.
Today, 22 of November 2016, South Korea called for many H5N6. Many cases were reported.
In November and December human cases of H5N6 were reported in China.
[5] In bird, by December there were four outbreaks in China since October and forced the culling of more than 170,000 birds.[6]
By December 2016 South Korea had raised its bird flu alert to highest level for the first time.[7] The heightened alarm status came as the country grappled with an outbreak of the highly pathogenic H5N6 bird flu that started a month ago in November. By the start of December H5N6 avian influenza was reported in bird droppings in Hong Kong.[8]

Aujeszky's disease(seudorabies) Aujeszky病(偽狂犬病)

Aujeszky's disease, usually called pseudorabies in the United States, is a viral disease in swine that has been endemic in most parts of the world. It is caused by Suid herpesvirus 1 (SuHV1). Aujeszky's disease is considered to be the most economically important viral disease of swine in areas where hog cholera has been eradicated.[1] Other mammals, such as humans,[2] cattle, sheep, goats, cats, dogs, and raccoons, are also susceptible. The disease is usually fatal in these animal species bar humans.[3]

The term "pseudorabies" is found inappropriate by many people, as SuHV1 is a herpesvirus and not related to the rabies virus.

Research on SuHV1 in pigs has pioneered animal disease control with genetically modified vaccines. SuHV1 is now used in model studies of basic processes during lytic herpesvirus infection, and for unravelling molecular mechanisms of herpesvirus neurotropism.[4][5]

Japanese encephalitis 日本腦炎

Japanese encephalitis (JE), formerly known as Japanese B encephalitis to distinguish it from Economo's A encephalitis—is a disease caused by the mosquito-borne Japanese encephalitis virus (JEV).[1]

The Japanese encephalitis virus (JEV) itself is a virus from the family Flaviviridae, part of the Japanese encephalitis serocomplex of 9 genetically and antigenically related viruses,[2] some which are particularly severe in horses, and four known to infect humans including West Nile virus.

Domestic pigs and wild birds (especially herons) are reservoirs of the virus; transmission to humans may cause severe symptoms. Amongst the most important vectors of this disease are the mosquitoes Culex tritaeniorhynchus and Culex vishnui. This disease is most prevalent in Southeast Asia, South Asia and East Asia.

Classical swine fever 典型豬瘟
Classical swine fever (CSF) or hog cholera (also sometimes called pig plague based on the German word Schweinepest) is a highly contagious disease of swine (Old World and New World pigs).[1]

The infectious agent responsible is a virus CSFV (previously called hog cholera virus) of the genus Pestivirus in the family Flaviviridae.[1][5] CSFV is closely related to the ruminant pestiviruses that cause bovine viral diarrhoea and border disease.[6]

The effect of different CSFV strains varies widely, leading to a wide range of clinical signs. Highly virulent strains correlate with acute, obvious disease and high mortality, including neurological signs and hemorrhages within the skin.

Less virulent strains can give rise to subacute or chronic infections that may escape detection, while still causing abortions and stillbirths. In these cases, herds in high-risk areas are usually serologically tested on a thorough statistical basis.

Infected piglets born to infected but subclinical sows help maintain the disease within a population. Other signs can include lethargy, fever, immunosuppression, chronic diarrhoea, and secondary respiratory infections. The incubation period of CSF ranges from 2 to 14 days, but clinical signs may not be apparent until after 2 to 3 weeks. Preventive state regulations usually assume 21 days

Bovine ephemeral fever 牛暫時熱
Bovine ephemeral fever (BEF) also known as Three Day Sickness is an arthropod vector-borne disease of cattle and is caused by bovine ephemeral fever virus (BEFV), a member of the genus Ephemerovirus in the family Rhabdoviridae.


BEFV forms a bullet- or cone-shaped virions that consist of a negative, single stranded RNA genome with a lipid envelope and 5 structural proteins. The envelope glycoprotein G contains type-specific and neutralizing antigenic sites. There has been recent evidence which demonstrated that BEFV induces apoptosis in several cell lines. It was however shown that apoptosis could be blocked by the caspase inhibitor (Z-VAD-fmk), indicating that BEFV induces caspase-dependent apoptosis in cultured cells.

Bovine herpesvirus 1 牛皰疹病毒1
Bovine herpesvirus 1 (BoHV-1) is a virus of the family Herpesviridae and the subfamily Alphaherpesvirinae, known to cause several diseases worldwide in cattle, including rhinotracheitis, vaginitis, balanoposthitis, abortion, conjunctivitis, and enteritis. BoHV-1 is also a contributing factor in shipping fever, also known as bovine respiratory disease (BRD). It is spread horizontally through sexual contact, artificial insemination, and aerosol transmission and it may also be transmitted vertically across the placenta. BoHV-1 can cause both clinical and subclinical infections, depending on the virulence of the strain. Although these symptoms are mainly non-life-threatening it is an economically important disease as infection may cause a drop in production and affect trade restrictions. Like other herpesviruses, BoHV-1 causes a lifelong latent infection and sporadic shedding of the virus. The sciatic nerve and trigeminal nerve are the sites of latency. A reactivated latent carrier is normally the source of infection in a herd. The clinical signs displayed are dependent on the virulence of the strain. There is a vaccine available which reduces the severity and incidence of disease. Some countries in Europe have successfully eradicated the disease by applying a strict culling policy.

Infectious bovine rhinotracheitis 傳染性牛鼻氣管炎
Infectious bovine rhinotracheitis

The respiratory disease caused by BoHV-1 is commonly known as infectious bovine rhinotracheitis. This disease affects the upper respiratory tract as well as the reproductive tract of cattle, and is commonly found in feedlots across North America.[1]

Clinical symptoms include fever, serous to mucopurulent nasal discharge, coughing, sneezing, difficulty breathing, conjunctivitis and loss of appetite. Ulcers commonly occur in the mouth and nose. Mortality may reach 10 percent.[5]

IBR can also cause abortion. This generally occurs in mid-gestation when a susceptible cow is infected with BoHV-1. A viraemia occurs and subsequently the virus crossed the placenta and causes organ necrosis in the fetus. BoHV-1 also causes a generalized disease in newborn calves, characterized by enteritis and death.

Porcine epidemic diarrhea virus

Porcine reproductive and respiratory syndrome virus

Porcine circovirus

Classical swine fever


Streptococcus suis


Actinobacillus pleuropneumoniae

Erysipelothrix rhusiopathiae

Pasteurella multocida








Porcine epidemic diarrhea virus 豬流行性腹瀉病毒

Porcine epidemic diarrhea virus (PED virus or PEDV) is a coronavirus that infects the cells lining the small intestine of a pig, causing porcine epidemic diarrhoea, a condition of severe diarrhea and dehydration. Older hogs mostly get sick and lose weight after being infected, where as newborn piglets usually die within five days of contracting the virus. PEDV cannot be transmitted to humans, nor contaminate the human food supply.

It was first discovered in Europe, but has become increasingly problematic in Asian countries, such as Korea, China, Japan, the Philippines, and Thailand. It has also spread to North America: it was discovered in the United States on May 5, 2013 in Indiana,[1] and in Canada in the winter of 2014. In January 2014, a new variant strain of PEDV with three deletions, one insertion, and several mutations in S (spike) 1 region was identified in Ohio by the Animal Disease Diagnostic Lab of Ohio Department of Agriculture.[2]

PEDV has a substantial economic burden given that it is highly infectious, resulting in significant morbidity and mortality in piglets. Morbidity and mortality rates were lower for vaccinated herds than for nonvaccinated herds, which suggests the emergence of a new PEDV field strain(s) for which the current vaccine, based on the CV777 strain, was partially protective.[3] Consumers are likely to feel the effects of the viral disease in the form of higher prices for pork products.[4]

Porcine reproductive and respiratory syndrome virus
Porcine reproductive and respiratory syndrome virus (PRRSV) is a virus that causes a disease of pigs, called porcine reproductive and respiratory syndrome (PRRS), also known as blue-ear pig disease (in Chinese, zhū láněr bìng 豬藍耳病). This economically important, panzootic disease causes reproductive failure in breeding stock and respiratory tract illness in young pigs. Initially referred to as "mystery swine disease" and "mystery reproductive syndrome," it was first reported in 1987 in North America (2) and Central Europe (3). The disease costs the United States swine industry around $644 million annually, and recent estimates in Europe found that it costs almost 1.5b€ every year.
Porcine Reproductive and Respiratory Syndrome (PRRS) is a complex disease. Modified Live Vaccines (MLV) vaccines are the primary immunological tool for its control, but PRRS control goes way beyond than just vaccination, and in order to achieve sustainable results, a systematic approach should be implemented. It requires a full understanding of the disease and a set of tools to achieve a long term success, therefore a standardized 5 step process
 has been developed to successfully achieve PRRS control. A strong platform to consolidate PRRS control in pig farms, large production systems and even geographical areas has been developed. This platform is a pig population approach having as main goals: - to maximize immunity, - reduce PRRS virus (PRRSv) exposure and - prevent new PRRSv infections. The Complexity of PRRS has allowed implementing successfully this methodology in the Swine Industry around the globe.

Porcine circovirus 豬圓環病毒

Porcine circovirus(PCV) is a single-stranded DNA virus (class II), that is nonenveloped with an unsegmented circular genome.[1] The viral capsid is icosahedral and approximately 17 nm in diameter. PCV is a member of the virus family Circoviridae.

PCVs are the smallest viruses replicating autonomously in eukaryotic cells.[2] They replicate in the nucleus of infected cells, using the host polymerase for genome amplification.

There are 2 strains: type 1 and type 2. Porcine Circovirus Associated Disease is caused by porcine circovirus type 2 (PCV2).[2]

PCV-1 (first identified in 1974) readily infects, but is not known to cause disease in swine; the type 2 has caused problems in recent years with the increasing occurrence of postweaning multisystemic wasting syndrome (PMWS), which over time results in significant depletion of lymphocytes; postmortem examination of diseased animals reveals enlarged lymph nodes and abnormal lung tissue.

Classical swine fever 典型豬瘟
Classical swine fever(CSF) or hog cholera (also sometimes called pig plague based on the German word Schweinepest) is a highly contagious disease of swine (Old World and New World pigs).[1]

The infectious agent responsible is a virus CSFV (previously called hog cholera virus) of the genus Pestivirus in the family Flaviviridae.[1][5] CSFV is closely related to the ruminant pestiviruses that cause bovine viral diarrhoea and border disease.[6]

The effect of different CSFV strains varies widely, leading to a wide range of clinical signs. Highly virulent strains correlate with acute, obvious disease and high mortality, including neurological signs and hemorrhages within the skin.

Less virulent strains can give rise to subacute or chronic infections that may escape detection, while still causing abortions and stillbirths. In these cases, herds in high-risk areas are usually serologically tested on a thorough statistical basis.

Infected piglets born to infected but subclinical sows help maintain the disease within a population. Other signs can include lethargy, fever, immunosuppression, chronic diarrhoea, and secondary respiratory infections. The incubation period of CSF ranges from 2 to 14 days, but clinical signs may not be apparent until after 2 to 3 weeks. Preventive state regulations usually assume 21 days

Streptococcus suis 鏈球菌

Streptococcus suis is a peanut-shaped, Gram-positive bacterium, and an important pathogen of pigs. Endemic in nearly all countries with an extensive pig industry, S. suis is also a zoonotic disease, capable of transmission to humans from pigs.[1]

Humans can be infected with S. suis when they handle infected pig carcasses or meat, especially with exposed cuts and abrasions on their hands. Human infection can be severe, with meningitis, septicaemia, endocarditis, and deafness as possible outcomes of infection.[2] Fatal cases of S. suis are uncommon, but not unknown.[1]

Penicillin is the most common antibiotic used in treatment of S. suis infection; in cases with cardiac involvement (endocarditis), gentamicin should also be given for synergistic effect.

Actinobacillus pleuropneumoniae 放線桿菌胸膜肺炎
Actinobacillus pleuropneumoniae (previously Haemophilus pleuropneumoniae), is a Gram-negative, facultative anaerobic, respiratory pathogen found in pigs. It was first reported in 1957, and was formally declared to be the causative agent of porcine pleuropneumonia in 1964.[1][2] It was reclassified in 1983 after DNA studies showed it was more closely related to A. lignieresii.[3]
A. pleuropneumoniae is a nonmotile, Gram-negative, encapsulated coccobacillus bacterium found in the Pasteurellaceae family.[4][5] It exhibits β-hemolysis activity,[6] thus explaining its growth on chocolate or blood agar, but must be supplemented with NAD ('V factor') to facilitate growth for one of its biological variants (biovar 1).[3] As a facultative anaerobic pathogen, A. pleuropneumoniae may need CO2 to grow.[3] Depending on the biovar, the bacteria may or may not be positive for urease; both biovars are positive for porphyrin.[3]

Erysipelothrix rhusiopathiae 豬丹毒絲狀菌

Erysipelothrix rhusiopathiae is a Gram-positive, catalase-negative, rod-shaped, nonspore-forming, nonacid-fast, nonmotile bacterium. The organism was first established as a human pathogen late in the 19th century.[1] It may be isolated from soil, food scraps, and water contaminated by infected animals. It can survive in soil for several weeks. In pig faeces, the survival period of this bacterium ranges from 1 to 5 months.[2] It grows aerobically and anaerobically and does not contain endotoxin. Distributed worldwide, E. rhusiopathiae is primarily considered an animal pathogen, causing a disease known as erysipelas in animals (and erysipeloid in humans – see below). Turkeys and pigs are most commonly affected, but cases have been reported in other birds, sheep, fish, and reptiles.[3] In pigs, the disease is known as "diamond skin disease". The human disease called erysipelas is not caused by E. rhusiopathiae, but by various members of the genus Streptococcus.

It is most frequently associated as an occupational disease of butchers.

Pasteurella multocida 多殺性巴斯德桿菌
Pasteurella multocida is a Gram-negative, nonmotile, penicillin-sensitive coccobacillus belonging to the Pasteurellaceae family.[1] Strains belonging to the species are currently classified into five serogroups (A, B, D, E, F) based on capsular composition and 16 somatic serovars (1-16). P. multocida is the cause of a range of diseases in mammals and birds, including fowl cholera in poultry, atrophic rhinitis in pigs, and bovine hemorrhagic septicemia in cattle and buffalo. It can also cause a zoonotic infection in humans, which typically is a result of bites or scratches from domestic pets. Many mammals (including domestic cats and dogs) and birds harbor it as part of their normal respiratory microbiota.
See: Pasteurellosis

P. multocida causes a range of diseases in wild and domesticated animals, as well as humans. The bacterium can be found in birds, cats, dogs, rabbits, cattle, and pigs. In birds, P. multocida causes avian or fowl cholera disease; a significant disease present in commercial and domestic poultry flocks worldwide, particularly layer flocks and parent breeder flocks. P. multocida strains that cause fowl cholera in poultry typically belong to the serovars 1, 3, and 4. In the wild, fowl cholera has been shown to follow bird migration routes, especially of snow geese. The P. multocida serotype-1 is most associated with avian cholera in North America, but the bacterium does not linger in wetlands for extended periods of time.[3] P. multocida causes atrophic rhinitis in pigs;[4] it also can cause pneumonia or bovine respiratory disease in cattle.[5][6] In humans, P. multocida is the most common cause of infection from wound infections after dog or cat bites. The infection usually shows as soft tissue inflammation within 24 hours. High leukocyte and neutrophil counts are typically observed, leading to an inflammatory reaction at the infection site (generally a diffuse, localized cellulitis).[7] It can also infect other locales, such as the respiratory tract, and is known to cause regional lymphadenopathy (swelling of the lymph nodes). In more serious cases, a bacteremia can result, causing an osteomyelitis or endocarditis. The bacteria may also cross the blood–brain barrier and cause meningitis.[8]

Pasteurella 巴氏桿菌

Pasteurella is a genus of Gram-negative, facultatively anaerobic bacteria.[1][2] Pasteurella species are nonmotile and pleomorphic, and often exhibit bipolar staining ("safety pin" appearance). Most species are catalase- and oxidase-positive.[3] The genus is named after the French chemist and microbiologist, Louis Pasteur, who first identified the bacteria now known as Pasteurella multocida as the agent of chicken cholera.

See also: Pasteurellosis

Many Pasteurella species are zoonotic pathogens, and humans can acquire an infection from domestic animal bites.[4][5] In cattle, sheep, and birds, Pasteurella species can cause a life-threatening pneumonia; in cats and dogs, however, Pasteurella is not a cause of disease, and constitutes part of the normal flora of the nose and mouth.[6] Pasteurella haemolytica is a species that infects mainly cattle and horses: P. multocida is the most frequent causative agent in human Pasteurella infection.[7] Common symptoms of pasteurellosis in humans include swelling, cellulitis, and bloody drainage at the site of the wound. Infection may progress to nearby joints, where it can cause further swelling, arthritis, and abscesses.[6]

Pasteurella spp. are generally susceptible to chloramphenicol, the penicillins, tetracycline, and the macrolides.[6]

The common occurrence of the bacteria is a reason to be medically proactive and defensive (antibacterial treatments are often necessary) if a bite occurs.[8]

coccidiosis 球蟲病

Coccidiosis is a parasitic disease of the intestinal tract of animals caused by coccidian protozoa. The disease spreads from one animal to another by contact with infected feces or ingestion of infected tissue. Diarrhea, which may become bloody in severe cases, is the primary symptom. Most animals infected with coccidia are asymptomatic, but young or immunocompromised animals may suffer severe symptoms and death.

While coccidia can infect a wide variety of animals, including humans, birds, and livestock, they are usually species-specific. One well-known exception is toxoplasmosis caused by Toxoplasma gondii.[1][2]

Humans may first encounter coccidia when they acquire a young puppy or kitten that is infected. Other than T. gondii, the infectious organisms are canine and feline-specific and are not contagious to humans, unlike the zoonotic diseases.

Listeria 李斯特菌

Listeria is a genus of bacteria that, until 1992, contained 10 known species,[1][2] each containing two subspecies. As of 2014, another five species were identified.[3] Named after the British pioneer of sterile surgery Joseph Lister, the genus received its current name in 1940. Listeria species are gram-positive, rod-shaped, and facultatively anaerobic, and do not produce endospores.[4] The major human pathogen in the Listeria genus is L. monocytogenes. It is usually the causative agent of the relatively rare bacterial disease listeriosis, a serious infection caused by eating food contaminated with the bacteria. The disease affects pregnant women, newborns, adults with weakened immune systems, and the elderly.

Listeriosis is a serious disease for humans; the overt form of the disease has a case-fatality rate around 20%. The two main clinical manifestations are sepsis and meningitis. Meningitis is often complicated by encephalitis, when it is known as meningoencephalitis, a pathology that is unusual for bacterial infections. L. ivanovii is a pathogen of mammals, specifically ruminants, and has rarely caused listeriosis in humans.[5]The incubation period can vary between 3 and 70 days.[6]

Listeriosis 李斯特菌病

Listeriosis is an infectious but not contagious disease caused by the bacterium Listeria monocytogenes, far more common in domestics animals (domestic mammals and poultry), especially ruminants, than in human beings. It can also occur in feral animals—among others, game animals—as well as in poultry and other birds.

The causative bacterium lives in the soil and in poorly made silage and is acquired by ingestion. It is not contagious; over the course of 30-year observation period of sheep disease in Morocco, the disease only appeared in the late 2000s (decade) when feeding bag-ensiled corn became common.[1] In Iceland, the disease is called "silage sickness".[2]

The disease is usually sporadic, but can occur as farm outbreaks in ruminants.

Three main forms are usually recognized throughout the affected species:

Listeriosis in animals can rarely be cured with antibiotics (tetracyclines, chloramphenicol and benzyl penicillin also) when diagnosed early, in goats, for example, by treating upon first noticing the disease's characteristic expression in the animal's face,[4] but is generally fatal.


Derzsy's disease is caused by a virus from the Parvoviridae family. It affects geese and Muscovy ducks.

The virus is shed in the faeces and thus transmission is horizontal, via the direct faecal-oral route and also indirectly via fomites. Vertical transmission is also possible.

Clinical disease only occurs in young geese and ducks between birth and 4–5 weeks of age.

Several genotypes have been described.[1] The genotype is based upon the sequence of the VP3 protein.
Clinical signs and diagnosis

Acute disease leads to death in most birds between the ages of 7–10 days. Clinical signs are quite limited in those cases. Older animals tend to show severe systemic and neurological signs and diarrhoea. Adults do not show any clinical signs.[2]

Viral isolation should be attempted for diagnosis, and immunofluorescence and electron microscopy can confirm the viral infection. Pathological changes may also help the diagnosis.[2]

 Toxoplasma gondii
弓形蟲 Vibrio Anguillarum
Vibrio harveyi
哈維弧菌 CpG Oligodeoxynucleotides CpG寡脫氧核苷酸
DNA vaccination
Toxoplasma gondii 弓形蟲

Toxoplasma gondii (IPA /ˈtɒksˌplæzmə ˈɡɒndi./) is an obligate intracellular, parasitic alveolate that causes the disease toxoplasmosis.[3] Found worldwide, T. gondii is capable of infecting virtually all warm-blooded animals,[4] but felids such as domestic cats are the only known definitive hosts in which the parasite can undergo sexual reproduction.[5]

In humans, T. gondii is one of the most common parasites in developed countries;[6][7] serological studies estimate that 30–50% of the global population has been exposed to and may be chronically infected with T. gondii, although infection rates differ significantly from country to country.[8][9] For example, previous estimates have shown the highest prevalence of persons infected to be in France, at 84%.[10] Although mild, flu-like symptoms occasionally occur during the first few weeks following exposure, infection with T. gondii produces no readily observable symptoms in healthy human adults.[8][11][12] This asymptomatic state of infection is referred to as a latent infection and has recently been associated with numerous subtle adverse or pathological behavioral alterations in humans.[8][13] In infants, HIV/AIDS patients, and others with weakened immunity, infection can cause a serious and occasionally fatal illness, toxoplasmosis.[11][12]

T. gondii has been shown to alter the behavior of infected rodents in ways thought to increase the rodents' chances of being preyed upon by cats.[10][14][15] 

Vibrio anguillarum 鰻弧菌
Vibrio anguillarum is a Gram-negative, curved-rod bacterium with one polar flagellum. It is an important pathogen of cultured salmonid fish, and causes the disease known as vibriosis or red pest of eels. The disease has been observed in salmon, bream, eel, mullet, catfish, and tilapia, amongst others. The organism is most prevalent in late summer in salt or brackish water and transmission is mainly horizontal by direct contact. It is widely distributed across the world.
Multiple haemorrhages in the body and skin changes signifying systemic involvement occur. Splenomegaly (enlargement of spleen) may be evident in young fish. Diagnosis relies on culture of V. anguillarum and the use of monoclonal antibodies.[1]
Treatment and control[edit]
Various antibiotics such as ampicillinchloramphenicolnalidixic acid derivatives, nitrofuranssulfonamides, and trimethoprim can be used to treat the fish. Resistance is emerging, however. A vaccine against V. anguillarum is available.

Vibrio harveyi 哈維弧菌
Vibrio harveyi is a Gram-negative, bioluminescent, marine bacterium in the genus Vibrio. V. harveyi is rod-shaped, motile (via polar flagella), facultatively anaerobic, halophilic, and competent for both fermentative and respiratory metabolism. It does not grow below 4 °C or above 35 °C. V. harveyi can be found free-swimming in tropical marine waters, commensally in the gut microflora of marine animals, and as both a primary and opportunistic pathogen of marine animals, including Gorgonian corals, oysters, prawns, lobsters, the common snook, barramundi, turbot, milkfish, and seahorses.[1] 
It is responsible for luminous vibriosis, a disease that affects commercially farmed penaeid prawns.[2] Additionally, based on samples taken by ocean-going ships, V. harveyi is thought to be the cause of the milky seas effect, in which, during the night, a uniform blue glow is emitted from the seawater. Some glows can cover nearly 6,000 sq mi (16,000 km2).
Quorum sensing[edit]
Groups of V. harveyi bacteria communicate by quorum sensing to coordinate the production of bioluminescence and virulence factors. Quorum sensing was first studied in V. fischeri (now Aliivibrio fischeri), a marine bacterium that uses a synthase (LuxI) to produce a species-specific autoinducer (AI) that binds a cognate receptor (LuxR) that regulates changes in expression. Coined "LuxI/R" quorum sensing, these systems have been identified in many other species of Gram-negative bacteria.[3] Despite its relatedness to A. fischeri, V. harveyi lacks a LuxI/R quorum-sensing system, and instead employs a hybrid quorum-sensing circuit, detecting its AI through a membrane-bound histidine kinase and using a phosphorelay to convert information about the population size to changes in gene expression.[4] Since their identification in V. harveyi, such hybrid systems have been identified in many other bacterial species. V. harveyi uses a second AI, termed autoinducer-2 or AI-2, which is unusual because it is made and detected by a variety of different bacteria, both Gram-negative and Gram-positive.[5][6][7] Thus, V. harveyi has been instrumental to the understanding and appreciation of interspecies bacterial communication.

CpG oligodeoxynucleotides CpG寡脫氧核苷酸
CpG oligodeoxynucleotides (or CpG ODN) are short single-stranded synthetic DNA molecules that contain a cytosine triphosphate deoxynucleotide ("C") followed by a guanine triphosphate deoxynucleotide ("G"). The "p" refers to the phosphodiester link between consecutive nucleotides, although some ODN have a modified phosphorothioate (PS) backbone instead. When these CpG motifs are unmethylated, they act as immunostimulants.[1] CpG motifs are considered pathogen-associated molecular patterns (PAMPs) due to their abundance in microbial genomes but their rarity in vertebrate genomes.[2] The CpG PAMP is recognized by the pattern recognition receptor (PRR) Toll-Like Receptor 9 (TLR9), which is constitutively expressed only in B cells and plasmacytoid dendritic cells (pDCs) in humans and other higher primates.[3]
Since 1893, it has been recognized that Coley's toxin, a mixture of bacterial cell lysate, has immunostimulatory properties that could reduce the progression of some carcinomas,[4] but it was not until 1983 that Tokunaga et al. specifically identified bacterial DNA as the underlying component of the lysate that elicited the response.[5] Then, in 1995 Krieg et al. demonstrated that the CpG motif within bacterial DNA was responsible for the immunostimulatory effects and developed synthetic CpG ODN.[6] Since then, synthetic CpG ODN have been the focus of intense research due to the Type I pro-inflammatory response they elicit and their successful use as vaccine adjuvants.
Structural Features[edit]
Synthetic CpG ODN differ from microbial DNA in that they have a partially or completely phosphorothioated (PS) backbone instead of the typical phosphodiester backbone and a poly G tail at the 3' end, 5' end, or both. PS modification protects the ODN from being degraded by nucleases such as DNase in the body and poly G tail enhances cellular uptake.[7] The poly G tails form intermolecular tetrads that result in high molecular weight aggregates. These aggregates are responsible for the increased activity the poly G sequence impart; not the sequence itself.[8] Numerous sequences have been shown to stimulate TLR9 with variations in the number and location of CpG dimers, as well as the precise base sequences flanking the CpG dimers. This led to the creation of five unofficial classes or categories of CpG ODN based on their sequence, secondary structures, and effect on human peripheral blood mononuclear cells (PBMCs). The five classes are Class A (Type D), Class B (Type K), Class C, Class P, and Class S.[9] It is important to note that during the discovery process, the "Classes" were not defined until much later when it became evident that ODN with certain characteristics elicited specific responses. Because of this, most ODN referred to in the literature use numbers (i.e., ODN 2006, ODN 2007, ODN 2216, ODN D35, ODN K3, etc.). The numbers are arbitrary and come from testing large numbers of ODN with slight variations in attempts to find the optimal sequence. In addition, some papers will give different names to previously described ODN, complicating the naming convention even more.

DNA vaccination DNA疫苗接種

DNA vaccination is a technique for protecting against disease by injection with genetically engineered DNA so cells directly produce an antigen, producing a protective immunological response. DNA vaccines have potential advantages over conventional vaccines, including the ability to induce a wider range of immune response types.
Several DNA vaccines are available for 
veterinary use. One DNA vaccine has been approved for human use. Research is investigating the approach for viral, bacterial and parasitic diseases in humans, as well as for several cancers.
Mechanism of plasmids[edit]
Once the plasmid inserts itself into the transfected cell nucleus, it codes for a peptide string of a foreign antigen. On its surface cell the displays the foreign antigen with both histocompatibility complex (MHC) classes I and class II molecules. The antigen-presenting cell then travels to the lymph nodes and presents the antigen peptide and costimulatory molecule signaled by T-cell, initiating the immune response.[18]
Vaccine insert design[edit]
Immunogens can be targeted to various cellular compartments to improve antibody or cytotoxic T-cell responses. Secreted or plasma membrane-bound antigens are more effective at inducing antibody responses than cytosolic antigens, while cytotoxic T-cell responses can be improved by targeting antigens for cytoplasmic degradation and subsequent entry into the major histocompatibility complex (MHC) class I pathway.[2] This is usually accomplished by the addition of N-terminal ubiquitin signals.[19][20][21]
The conformation of the protein can also affect antibody responses. “Ordered” structures (such as viral particles) are more effective than unordered structures.[22] Strings of minigenes (or MHC class I epitopes) from different pathogens raise cytotoxic T-cell responses to some
pathogens, especially if a TH epitope is also included


Diagnostic kit
Monoclonal antibody, Rapid test strip, Test reagent kit for Avian , Swine , Bovine , Dog and Feline diseases, etc.


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