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Canine distemper
Canine distemper is a very serious viral disease that affects animals in the families Canidae, Mustelidae, Mephitidae, Hyaenidae, Ailuridae, Procyonidae, Pinnipedia, some Viverridae and Felidae (though not domestic cats; feline distemper or panleukopenia is a different virus exclusive to cats). It is most commonly associated with domestic animals such as dogs, although ferrets are also vaccinated for it. It is a single-stranded RNA virus of the family paramyxovirus, and thus a close relative of measles and rinderpest.Despite extensive vaccination in many regions, it remains a major disease of dogs
Etymology
The origin of the word distemper is from the Middle English distemperen, meaning to upset the balance of the humors, which is from the Old French destemprer, meaning to disturb, which is from the Vulgar Latin distemperare: Latin dis- and Latin temperare, meaning to not mix properly
HistoryAlthough very similar to the measles virus, CDV seems to have appeared more recently, with the first case described in 1905 by French veterinarian Henri Carré. It was first thought to be related to the Plague and Typhus and resulted from several species of bacteria. It now affects all populations of domestic dog and some populations of wildlife. A vaccine was developed in 1950, yet due to limited use the virus remains prevalent in many populations. The domestic dog has largely been responsible for introducing canine distemper to previously unexposed wildlife and now causes a serious conservation threat to many species of carnivores and some species of marsupials. The virus contributed to the near-extinction of the black-footed ferret. It also may have played a considerable role in the extinction of the Tasmanian tiger and recurrently causes mortality among African wild dogs In 1991, the lion population in Serengeti, Tanzania experienced a 20% decline as a result of the disease. The disease has also mutated to form phocid distemper virus, which affects seals.
Infection
A. Lung lesion in an African Wild Dog B. Viral inclusion bodiesPuppies from three to six months old are particularly susceptible. Canine distemper virus (CDV) spreads through the aerosol droplets and through contact with infected bodily fluids including nasal and ocular secretions, feces, and urine 6–22 days after exposure. It can also be spread by food and water contaminated with these fluids. The time between infection and disease is 14 to 18 days, although there can be a fever from three to six days postinfection.
Canine distemper virus tends to orient its infection towards the lymphoid, epithelial, and nervous tissues. The virus initially replicates in the lymphatic tissue of the respiratory tract. The virus then enters the blood stream and infects the lymphatic tissue followed by respiratory, Gastrointestinal, urogenital epithelium, the Central Nervous System, and optic nerves. Therefore, the typical pathologic features of canine distemper include lymphoid depletion (causing immunosuppression and leading to secondary infections), interstitial pneumonia, encephalitis with demyelination, and hyperkeratosis of foot pads.
The mortality rate of the virus largely depends on the immune status of the infected dogs. Puppies experience the highest mortality rate where complications such as pneumonia and encephalitis are more common. In older dogs that do develop distemper encephalomyetilis, vestibular disease may present. Around 15% of canine inflammatory central nervous system diseases are a result of CDV
Disease progression
The virus first appears in bronchial lymph nodes and tonsils two days after exposure. The virus then enters the blood stream on the second or third day. In older dogs that do develop distemper encephalomyetilis, vestibular disease may present. A first round of acute fever tends to begin around 3 to 8 days after infection which is often accompanied by a low white blood cell count, especially of lymphocytes as well as low platelet count. These signs may or may not be accompanied by anorexia, a runny nose, and discharge from the eye. This first round of fever typically recedes rapidly within 96 hours and then a second round of fever begins around the 11th or 12th day and lasts at least a week. Gastrointestinal and respiratory problems tend to follow which may become complicated with secondary bacterial infections. Inflammation of the brain and spinal cord otherwise known as encephalomyelitis is either associated with this, subsequently follows, or comes completely independent of these problems. A thickening of the footpads sometimes develops and vesicularpustular lesions on the abdomen usually develop. Neurological symptoms typically are found in the animals with thickened footpads from the virus About half of sufferers experience meningoencephalitis.
Gastrointestinal and respiratory symptomsCommonly observed signs are a runny nose, vomiting and diarrhea, dehydration, excessive salivation, coughing and/or labored breathing, loss of appetite, and weight loss. When and if the neurological symptoms develop, urination and defecation may become involuntary.
Neurological symptomsThe symptoms within the central nervous system include a localized involuntary twitching of muscles or groups of muscles, seizures often distinguished by salivation and jaw movements commonly described as “chewing gum fits,” or more appropriately as "distemper myoclonus." As the condition progresses, the seizures worsen and advance to grand mal convulsions, followed by death of the animal. The animal may also show signs of sensitivity to light, incoordination, circling, increased sensitivity to sensory stimuli such as pain or touch, and deterioration of motor capabilities. Less commonly it may lead to blindness and paralysis. The length of the systemic disease may be as short as 10 days, or the start of neurological symptoms may not come until several weeks or months later. Those few that survive usually have a small tic or twitch of varying levels of severity. With time this tic will usually diminish somewhat in its severity.
Diagnosis
The above symptoms, especially fever, respiratory signs, neurological signs, and thickened footpads found in unvaccinated dogs strongly indicate canine distemper. However, several febrile diseases match many of the symptoms of the disease and only recently has differing between canine hepatitis, herpes virus, parainfluenza and leptospirosis been possible.Thus, finding the virus by various methods in the dog's conjunctival cells gives a definitive diagnosis. In older dogs that develop distemper encephalomyetilis, diagnosis may be more difficult since many of these dogs have an adequate vaccination history
The most reliable test to confirm distemper is a Brush Border slide/smear of the bladder transitional epithelium of the inside lining from the bladder, stained with Dif-Quick. These cells will always have inclusions. Inclusions in these cells which will stain a carmine red color and be para nuclear in the cytoplasm of infected cells. About 90% of the bladder cells will be positive for inclusions in the early stages of distemper. This is good for at least the first 21 days from onset of the disease. After this point, it gets harder to detect as the disease progresses further in the stages and the physical clinical signs will become quite obvious.[citation needed]
Prevention
See also: DA2PPC Vaccine
There exist a number of vaccines against canine distemper for dogs (ATCvet code: QI07AD05 and combinations) and domestic ferrets (QI20DD01), which in many jurisdictions are mandatory for pets. The type of vaccine should be approved for the type of animal being inoculated, or else the animal could actually contract the disease from the vaccine. A dog who has eaten meat infected with Rinderpest can also sometimes receive temporary immunity.Infected animals should be quarantined from other dogs for several months due to the length of time the animal may shed the vires. The virus is destroyed in the environment by routine cleaning with disinfectants, detergents, or drying. It does not survive in the environment for more than a few hours at room temperature (20–25 °C), but can survive for a few weeks in shady environments at temperatures slightly above freezing. It, along with other labile viruses, can also persist longer in serum and tissue debris
Treatment
Until recently, canine distemper has been associated with a long history of pessimism with respect to treatment of infected animals and the disease was usually assumed to have a poor prognosis. Most care offered was only palliative, geared toward easing the suffering. Several factors had an important role in maintaining the status quo.
Misdiagnosis, miseducation, a lack of treatment, inadequate, or inappropriate treatment has historically created barriers and slowed the development of effective solutions to the disease. Even today the needs of affected animals often go unrecognized until the disease reaches the nervous stage and the distressed behavior and/or impaired functional state of the animal is more obvious and less responsive to treatment.
Research and funding for the most part have focused on preventative vaccination rather than on finding a cure for distemper.
Another factor is the outdated theory that the injuries that occurred were the result of a strictly autoimmune reaction, the thought being that initially the canine distemper virus was introduced, then subsequently eliminated, but that cytokines continued to attack and damage healthy tissue in the absence of a current pathogen. Based on that faulty assumption, anti-inflammatory and immunosuppressive drugs have been prescribed by some veterinarians in an attempt to bring the effects of the condition under control.
It was later considered that the action of macrophages on nerve cells is targeted on infected cells, indicating that the autoimmune reaction is likely a direct consequence of the presence of the virus Often, owners seek expert help only when the disease is in its advanced stages (nervous phase) and prescription anti-inflammatory drugs (which are usually corticosteroids) undermine the immune system of the animal, allow the proliferation of the virus, and the autoimmune reaction increases as a means of containment of infected cells.
The most successful treatments for canine distemper are adaptations of established treatments used for other diseases caused by similar viruses, such as Ribavirin and vitamin A, which are used to treat measles, the same family and gender (Paramyxoviridae - morbillivirus) and Interferon Alpha, used for the treatment of measles and a vaccine used to immunize birds against Newcastle disease same family but different genera (Paramyxoviridae - AVULAVIRUS).
The first references that suggested effective treatments for similar viruses could be effective for canine distemper arose when studies found that canine distemper was a disease comparable to measles and infected animals could be used to develop new technologies for treatment of measles. The question of whether the reciprocal would be true was cleared when studies assessed the efficacy of traditional treatments for measles which were then successfully applied to animals with distemper.
The first finding was when the induction of high levels of Vitamin A, which is a ostensibly treatment used to treat measles (including being recommended by the World Health Organization), produced an effect of 100% cure in animals experimentally infected. The group that received no supplementation all died. . Currently, it is known that the direct inhibitor effect of retinoids (Vitamin A and subproducts) over the measles virus is what confirms the choice of Vitamin A as a treatment for canine distemper
The confirmation of the effectiveness of Vitamin A in the treatment of canines, especially dogs, is its ability to convert the Vitamin A into nontoxic esters This characteristic of carnivores is well known, which removes the risk of hypervitaminosis possible due to the maintenance of high doses. For dogs there is a benchmark to measure the risk of hypervitaminosis, a national research found that it takes a dose of 300,000 IU / kg daily for thirty days so that the first signs of hypervitaminosis appear, and need sixty days of ingestion at this dosage to kill the animal Since this dosage, 300,000 IU / kg is sixty times greater than the limit established for humans.
The mechanisms of action that explain its effectiveness in the treatment of distemper remain unexplained, and this issue also exists for the case of measles. Some evidence points to an indirect action, such as checking that there is a reduction in the amounts of Vitamin A during infection, pointing to the hypothesis that [ [Vitamin A]] is raw material for some mechanism of resistance to infection. The very characteristic antiinfectiva not specific Vitamin A is a mystery, however there was any doubt about its effectiveness, action mechanisms elucidated or not.
The adoption of Ribavirin as a treatment for canine followed the same steps of Vitamin A, it was the principle used in cases of subacute sclerosing panencephalitis under measles. The first verification of the effectiveness occurred in vitro. What was observed was that the distemper virus is very susceptible to Ribavirin and its mechanism of induction error catastrophe are needed from 0.02 to 0.05 micro mols to create an inhibitory effect on virus replication by 50%.
The main concern in the use of Ribavirin was the result of its interaction with the blood-brain barrier. Being the brain a immunologically privileged area, the concerns was the capacity of Ribavirin to overcome this barrier. A study using mice with encephalitis due to measles it was found that once the virus has become established in phase nervosa, the blood-brain barrier in a way fails, reducing the restriction to the action of the Ribavirin in these areas. The verification of all these results in vivo resulted in an effectiveness of 80% in animals that had already reached the nervous phase of viral infection. The application of Ribavirin demands a close monitoring of the animal due the risk of leukopenia and the ingestion of log-chain tryglicerides(in other words: fats) in order to better absorb the drug and for preservation of gastric region, which are quite susceptible to Ribavirin.[dubious – discuss]
Canine distemper virus and Paget's disease
Paget's disease, a focal destructive disease of bone, has long suspected paramyxoviruses such as CDV, measles, respiratory syncytial virus, simian virus 5, and parainfluenza virus Type 3 as a culprit. Most studies, however, have pointed more directly at CDV and Measles.[33][34][35] The virus detection technique in situ-RT-PCR has shown CDV in 100% of Pagetic samples whereas other virus detection techniques have been less accurate
Etymology
The origin of the word distemper is from the Middle English distemperen, meaning to upset the balance of the humors, which is from the Old French destemprer, meaning to disturb, which is from the Vulgar Latin distemperare: Latin dis- and Latin temperare, meaning to not mix properly
HistoryAlthough very similar to the measles virus, CDV seems to have appeared more recently, with the first case described in 1905 by French veterinarian Henri Carré. It was first thought to be related to the Plague and Typhus and resulted from several species of bacteria. It now affects all populations of domestic dog and some populations of wildlife. A vaccine was developed in 1950, yet due to limited use the virus remains prevalent in many populations. The domestic dog has largely been responsible for introducing canine distemper to previously unexposed wildlife and now causes a serious conservation threat to many species of carnivores and some species of marsupials. The virus contributed to the near-extinction of the black-footed ferret. It also may have played a considerable role in the extinction of the Tasmanian tiger and recurrently causes mortality among African wild dogs In 1991, the lion population in Serengeti, Tanzania experienced a 20% decline as a result of the disease. The disease has also mutated to form phocid distemper virus, which affects seals.
Infection
A. Lung lesion in an African Wild Dog B. Viral inclusion bodiesPuppies from three to six months old are particularly susceptible. Canine distemper virus (CDV) spreads through the aerosol droplets and through contact with infected bodily fluids including nasal and ocular secretions, feces, and urine 6–22 days after exposure. It can also be spread by food and water contaminated with these fluids. The time between infection and disease is 14 to 18 days, although there can be a fever from three to six days postinfection.
Canine distemper virus tends to orient its infection towards the lymphoid, epithelial, and nervous tissues. The virus initially replicates in the lymphatic tissue of the respiratory tract. The virus then enters the blood stream and infects the lymphatic tissue followed by respiratory, Gastrointestinal, urogenital epithelium, the Central Nervous System, and optic nerves. Therefore, the typical pathologic features of canine distemper include lymphoid depletion (causing immunosuppression and leading to secondary infections), interstitial pneumonia, encephalitis with demyelination, and hyperkeratosis of foot pads.
The mortality rate of the virus largely depends on the immune status of the infected dogs. Puppies experience the highest mortality rate where complications such as pneumonia and encephalitis are more common. In older dogs that do develop distemper encephalomyetilis, vestibular disease may present. Around 15% of canine inflammatory central nervous system diseases are a result of CDV
Disease progression
The virus first appears in bronchial lymph nodes and tonsils two days after exposure. The virus then enters the blood stream on the second or third day. In older dogs that do develop distemper encephalomyetilis, vestibular disease may present. A first round of acute fever tends to begin around 3 to 8 days after infection which is often accompanied by a low white blood cell count, especially of lymphocytes as well as low platelet count. These signs may or may not be accompanied by anorexia, a runny nose, and discharge from the eye. This first round of fever typically recedes rapidly within 96 hours and then a second round of fever begins around the 11th or 12th day and lasts at least a week. Gastrointestinal and respiratory problems tend to follow which may become complicated with secondary bacterial infections. Inflammation of the brain and spinal cord otherwise known as encephalomyelitis is either associated with this, subsequently follows, or comes completely independent of these problems. A thickening of the footpads sometimes develops and vesicularpustular lesions on the abdomen usually develop. Neurological symptoms typically are found in the animals with thickened footpads from the virus About half of sufferers experience meningoencephalitis.
Gastrointestinal and respiratory symptomsCommonly observed signs are a runny nose, vomiting and diarrhea, dehydration, excessive salivation, coughing and/or labored breathing, loss of appetite, and weight loss. When and if the neurological symptoms develop, urination and defecation may become involuntary.
Neurological symptomsThe symptoms within the central nervous system include a localized involuntary twitching of muscles or groups of muscles, seizures often distinguished by salivation and jaw movements commonly described as “chewing gum fits,” or more appropriately as "distemper myoclonus." As the condition progresses, the seizures worsen and advance to grand mal convulsions, followed by death of the animal. The animal may also show signs of sensitivity to light, incoordination, circling, increased sensitivity to sensory stimuli such as pain or touch, and deterioration of motor capabilities. Less commonly it may lead to blindness and paralysis. The length of the systemic disease may be as short as 10 days, or the start of neurological symptoms may not come until several weeks or months later. Those few that survive usually have a small tic or twitch of varying levels of severity. With time this tic will usually diminish somewhat in its severity.
Diagnosis
The above symptoms, especially fever, respiratory signs, neurological signs, and thickened footpads found in unvaccinated dogs strongly indicate canine distemper. However, several febrile diseases match many of the symptoms of the disease and only recently has differing between canine hepatitis, herpes virus, parainfluenza and leptospirosis been possible.Thus, finding the virus by various methods in the dog's conjunctival cells gives a definitive diagnosis. In older dogs that develop distemper encephalomyetilis, diagnosis may be more difficult since many of these dogs have an adequate vaccination history
The most reliable test to confirm distemper is a Brush Border slide/smear of the bladder transitional epithelium of the inside lining from the bladder, stained with Dif-Quick. These cells will always have inclusions. Inclusions in these cells which will stain a carmine red color and be para nuclear in the cytoplasm of infected cells. About 90% of the bladder cells will be positive for inclusions in the early stages of distemper. This is good for at least the first 21 days from onset of the disease. After this point, it gets harder to detect as the disease progresses further in the stages and the physical clinical signs will become quite obvious.[citation needed]
Prevention
See also: DA2PPC Vaccine
There exist a number of vaccines against canine distemper for dogs (ATCvet code: QI07AD05 and combinations) and domestic ferrets (QI20DD01), which in many jurisdictions are mandatory for pets. The type of vaccine should be approved for the type of animal being inoculated, or else the animal could actually contract the disease from the vaccine. A dog who has eaten meat infected with Rinderpest can also sometimes receive temporary immunity.Infected animals should be quarantined from other dogs for several months due to the length of time the animal may shed the vires. The virus is destroyed in the environment by routine cleaning with disinfectants, detergents, or drying. It does not survive in the environment for more than a few hours at room temperature (20–25 °C), but can survive for a few weeks in shady environments at temperatures slightly above freezing. It, along with other labile viruses, can also persist longer in serum and tissue debris
Treatment
Until recently, canine distemper has been associated with a long history of pessimism with respect to treatment of infected animals and the disease was usually assumed to have a poor prognosis. Most care offered was only palliative, geared toward easing the suffering. Several factors had an important role in maintaining the status quo.
Misdiagnosis, miseducation, a lack of treatment, inadequate, or inappropriate treatment has historically created barriers and slowed the development of effective solutions to the disease. Even today the needs of affected animals often go unrecognized until the disease reaches the nervous stage and the distressed behavior and/or impaired functional state of the animal is more obvious and less responsive to treatment.
Research and funding for the most part have focused on preventative vaccination rather than on finding a cure for distemper.
Another factor is the outdated theory that the injuries that occurred were the result of a strictly autoimmune reaction, the thought being that initially the canine distemper virus was introduced, then subsequently eliminated, but that cytokines continued to attack and damage healthy tissue in the absence of a current pathogen. Based on that faulty assumption, anti-inflammatory and immunosuppressive drugs have been prescribed by some veterinarians in an attempt to bring the effects of the condition under control.
It was later considered that the action of macrophages on nerve cells is targeted on infected cells, indicating that the autoimmune reaction is likely a direct consequence of the presence of the virus Often, owners seek expert help only when the disease is in its advanced stages (nervous phase) and prescription anti-inflammatory drugs (which are usually corticosteroids) undermine the immune system of the animal, allow the proliferation of the virus, and the autoimmune reaction increases as a means of containment of infected cells.
The most successful treatments for canine distemper are adaptations of established treatments used for other diseases caused by similar viruses, such as Ribavirin and vitamin A, which are used to treat measles, the same family and gender (Paramyxoviridae - morbillivirus) and Interferon Alpha, used for the treatment of measles and a vaccine used to immunize birds against Newcastle disease same family but different genera (Paramyxoviridae - AVULAVIRUS).
The first references that suggested effective treatments for similar viruses could be effective for canine distemper arose when studies found that canine distemper was a disease comparable to measles and infected animals could be used to develop new technologies for treatment of measles. The question of whether the reciprocal would be true was cleared when studies assessed the efficacy of traditional treatments for measles which were then successfully applied to animals with distemper.
The first finding was when the induction of high levels of Vitamin A, which is a ostensibly treatment used to treat measles (including being recommended by the World Health Organization), produced an effect of 100% cure in animals experimentally infected. The group that received no supplementation all died. . Currently, it is known that the direct inhibitor effect of retinoids (Vitamin A and subproducts) over the measles virus is what confirms the choice of Vitamin A as a treatment for canine distemper
The confirmation of the effectiveness of Vitamin A in the treatment of canines, especially dogs, is its ability to convert the Vitamin A into nontoxic esters This characteristic of carnivores is well known, which removes the risk of hypervitaminosis possible due to the maintenance of high doses. For dogs there is a benchmark to measure the risk of hypervitaminosis, a national research found that it takes a dose of 300,000 IU / kg daily for thirty days so that the first signs of hypervitaminosis appear, and need sixty days of ingestion at this dosage to kill the animal Since this dosage, 300,000 IU / kg is sixty times greater than the limit established for humans.
The mechanisms of action that explain its effectiveness in the treatment of distemper remain unexplained, and this issue also exists for the case of measles. Some evidence points to an indirect action, such as checking that there is a reduction in the amounts of Vitamin A during infection, pointing to the hypothesis that [ [Vitamin A]] is raw material for some mechanism of resistance to infection. The very characteristic antiinfectiva not specific Vitamin A is a mystery, however there was any doubt about its effectiveness, action mechanisms elucidated or not.
The adoption of Ribavirin as a treatment for canine followed the same steps of Vitamin A, it was the principle used in cases of subacute sclerosing panencephalitis under measles. The first verification of the effectiveness occurred in vitro. What was observed was that the distemper virus is very susceptible to Ribavirin and its mechanism of induction error catastrophe are needed from 0.02 to 0.05 micro mols to create an inhibitory effect on virus replication by 50%.
The main concern in the use of Ribavirin was the result of its interaction with the blood-brain barrier. Being the brain a immunologically privileged area, the concerns was the capacity of Ribavirin to overcome this barrier. A study using mice with encephalitis due to measles it was found that once the virus has become established in phase nervosa, the blood-brain barrier in a way fails, reducing the restriction to the action of the Ribavirin in these areas. The verification of all these results in vivo resulted in an effectiveness of 80% in animals that had already reached the nervous phase of viral infection. The application of Ribavirin demands a close monitoring of the animal due the risk of leukopenia and the ingestion of log-chain tryglicerides(in other words: fats) in order to better absorb the drug and for preservation of gastric region, which are quite susceptible to Ribavirin.[dubious – discuss]
Canine distemper virus and Paget's disease
Paget's disease, a focal destructive disease of bone, has long suspected paramyxoviruses such as CDV, measles, respiratory syncytial virus, simian virus 5, and parainfluenza virus Type 3 as a culprit. Most studies, however, have pointed more directly at CDV and Measles.[33][34][35] The virus detection technique in situ-RT-PCR has shown CDV in 100% of Pagetic samples whereas other virus detection techniques have been less accurate
Parvovirus
WHAT IS PARVOVIRUS?
Canine Parvovirus is a viral disease of dogs that was first reported in early 1978. Parvovirus is capable of causing two different sets of clinical problems. The first to be recognized, and most common, is the “intestinal” form, which is manifested by diarrhea; often bloody vomiting, loss of appetite, depression, fever, and sometimes death. The second syndrome, the “cardiac” form, occurs in very young pups and is manifested by an acute inflammation of the heart muscle.
Any age, breed or sex of dog could be affected by Parvovirus. However, infection with Parvovirus does not automatically mean illness. Several factors such as age, environment, stress, parasites and general health status of each individual dog infected could affect the severity of illness. The degree of illness could range from very mild to unapparent to very severe, often resulting in death. The disease is usually more severe in young dogs (less than 6 months of age) or old dogs. Doberman pinschers and Rottweilers are breeds that are more susceptible to parvovirus.
WHERE DID IT COME FROM?
Experts agree that canine Parvovirus is closely related to Parvoviruses that affect other animals. Where the virus originally came from remains unknown, but it is possible that it is a mutant from another Parvovirus that affects other species of animals. Man is not known to be affected by canine Parvovirus. Since its first appearance in 1978, canine Parvovirus has spread to every continent in the world, probably the result of the hardy nature of the virus. It is resistant to extremes of temperature (i.e., it survives freezing and extreme heat) and is unharmed by detergents, alcohols and common disinfectants. Direct transmission occurs when an infected dog comes in contact with a healthy dog. The virus is found in heavy concentration in the infected dog’s stool. The virus particles can be easily spread on shoes, clothing and other inanimate objects. Fleas, as well as people, can therefore act as indirect sources of infection.
Oral Phase:
The disease process begins with the oral ingestion of Parvovirus from the feces of an infected dog. The virus initially invades the lymph glands of the throat (lymph nodes and tonsils) where it multiplies. Following multiplication in the lymph glands for l to 2 days, the virus then enters the blood stream, which causes the VIREMIA phase (virus in the blood).
Viremia Phase:
This phase is characterized by massive amounts of virus in the dog’s bloodstream, which in turn is spread to all parts of the body, such as, the intestine, bone marrow, spleen, other lymph nodes and the heart (in young pups less than 8 weeks of age). As infection spreads, the symptoms of illness become apparent. (See “symptoms” in next section). The Viremia phase can last for approximately l to 9 days.
Contagious Stage:
The final phase in the cycle is the contagious or “shedding” phase. As many as 30 billion Parvovirus particles can be shed from the intestines of an infected dog in every ounce of stool. The highest concentration of virus in the stool is seen when the infected dog is showing signs of illness. A dog can, however, be a source of infection to other dogs without having observable signs of illness. Transmission can occur for at least 3 weeks after a dog becomes infected with the virus. Chronic “carriers” are not know to exist as in other virus disease. Parvovirus in the environment can infect susceptible dogs for many months once shed in the stool.
WHAT ARE THE SYMPTOMS?
The symptoms below indicate a problem warranting medical attention. Early, vigorous treatment of illness caused by canine Parvovirus infection is imperative since vomiting and diarrhea can lead to dehydration and chemical imbalance in the body. If your dog shows these signs, see your veterinarian. Early treatment can save lives.
Cardiac Form
- Sudden death
- Crying, difficulty breathing, gasping for breath
- Extreme depression
- Weakness
- Unwillingness to nurse
- Irregular heartbeat
Intestinal Form (any age dog affected, but more severe in puppies).
- Depression
- Loss of appetite
- Fever (above 103 degrees F)
- Vomiting
- Diarrhea with or without blood (more serious if blood present)
- Low white blood count
HOW IS IT CONTROLLED?
Control of Parvovirus by sanitation measures alone is extremely difficult because the virus is such a resistant, hardy organism and because it is so easily spread. Contact with other dogs and especially their stool, should be minimized. Clorox diluted one part to 30 parts with water has been effective in disinfecting inanimate objects such as clothing, floors, kennels, etc. However, it is impractical, if not impossible, to disinfect public streets, parks, etc. Isolation of infected dogs is another method of control, although moderately effective. Both of these measures will help reduce the amount of contagious virus in the environment, but only vaccination will control the actual source of infection, the contagious shedding dog.
Vaccination:
The most effective control measure for canine Parvovirus disease. A properly immunized dog will have circulating antibodies in the blood that will destroy Parvovirus following exposure.
THE ROLE OF MATERNAL ANTIBODY IN PUPPY IMMUNIZATION:
Maternal antibodies are antibodies against Parvovirus, which are passed from the mother to the puppies through the “first milk” or colostrum. They provide the puppy with an immediate temporary or “passive” immunity. The mother obtains these antibodies from prior vaccination or by natural exposure to Parvovirus. However, maternal antibody is a two-edged sword; it protects the puppy against disease early in life, but it also blocks active immunization. In the case of Parvovirus, maternal antibody can interfere with vaccination for as long as 14 to 16 weeks of age in some pups. A refractory period can exist in some pups where very low, almost undetectable levels of maternal antibody will inhibit the vaccination process but will not prevent Parvovirus infection. Since the level of maternal antibody varies from puppy to puppy, it is important to begin vaccination at an early age and repeat every 2-3 weeks until the puppy is at least 16 - 18 weeks old.
Struktur sel Bakteri
Bakteri sebagai organisme prokariotik yang merupakan organisme uniseluler memiliki struktur sel yang tidak memiliki membran inti. Struktur sel secara umum yang dimiliki oleh sel prokariot dapat kita lihat pada sel bakteri.
Struktur Sel Bakteri
Nukleoid (Nukleus).Nukleus atau inti sel berfungsi sebagai pengendali dan pengatur sel. seluruh aktifitas sel diatur oleh nukleus. Nukleus juga berfungsi sebagai pembawa informasi genetik yaitu kromosom, yang diwariskan ke generasi selanjutnya. Kromosom adalah struktur yang tersusun oleh molekul DNA dan protein (histon). Nukleus sel bakteri terpapar atau kontak langsung dengan sitoplasma karena tidak memiliki membran inti.
Cytoplasm (Sitoplasma). Sitoplasma adalah bagian sel yang berisi cairan tempat berlangsungnya metabolisme sel. Kandungan terbesar dalam sitoplasma adalah air (80-90%).
Ribosome (Ribosom). Ribosom merupakan struktur berupa butiran-butiran kecil yaang merupakan tempat sintesis protein. Protein disintesis atau dibuat dengan menggabungkan beberapa asam amino yang sesuai informasi genetik yang ada di molekul DNA. Ribosom berada di sitoplasma.
Cytoplasmic membrane (Membran Plasma). Membran plasma adalah lapisan di luar sitoplasma yang tersusun atas phospolipid bilayer. Fungsi membran plasma adalah sebagai pelindung dan mengatur transportasi sel. Pengaturan transportasi sel dimasksudkan untuk mengatur keluar masuknya substansi ke dalam dan ke luar sel. Membran plasma juga berperan dalam penerima rangsang yang datang dari luar sel.
Ribosome (Ribosom). Ribosom merupakan struktur berupa butiran-butiran kecil yaang merupakan tempat sintesis protein. Protein disintesis atau dibuat dengan menggabungkan beberapa asam amino yang sesuai informasi genetik yang ada di molekul DNA. Ribosom berada di sitoplasma.
Cytoplasmic membrane (Membran Plasma). Membran plasma adalah lapisan di luar sitoplasma yang tersusun atas phospolipid bilayer. Fungsi membran plasma adalah sebagai pelindung dan mengatur transportasi sel. Pengaturan transportasi sel dimasksudkan untuk mengatur keluar masuknya substansi ke dalam dan ke luar sel. Membran plasma juga berperan dalam penerima rangsang yang datang dari luar sel.
Membran sel pada sel prokariot mengalami pelekukan ke arah dalam membentuk struktur yang disebut mesosome (mesosom). Mesosom berfungsi sebagai tempat terjadinya respirasi sel sehingga dihasilkan energi yang akan digunakan untuk aktifitas di dalam sel.
Cell wall (Dinding Sel). Dinding sel adalah struktur pelindung kedua setelah membran plasma.
Cell wall (Dinding Sel). Dinding sel adalah struktur pelindung kedua setelah membran plasma.
Capsule (Kapsul). Kapsul adalah struktur pelindung sel ketiga setelah membran plasma dan dinding sel.
Pili (Bulu Rambut). Pili berfungsi sebagai alat pelekatan sel bakteri pada suatu permukaan substrat atau benda. Flagella (Flagel). Flagel berfungsi dalam pergerakan sel. Baik flagel dan pili disusun oleh mikrotubulus.
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