Leptospirosis in dogs

Leptospirosis is a bacterial disease that affects many species of animals as well as human beings. Leptospirosis occurs throughout the World. The organism belongs to a phylum called spirochaetes, distinctive bacteria with long, helically coiled bodies. They can be recognized by the presence of flagella or ribbons running lengthwise down the cell and called axial filaments. These filament causes a twisting, spiral motion as the organism moves about. Most spirochaetes are free-living without oxygen (anaerobic) with only the Leptospira, the Borrelia of Lyme disease and the Treponema of human syphilis causing disease.

There are approximately 230 serologically distinct forms of the genus and species, Leptospira interrogans, which are called serovars. Nine serovars are known to cause disease in dogs. They are Leptospira icterohaemorrhagiae, L. canicola, L. grippotyphosa, L. pomona, L. bratislava, L. automnalis, L. bataviae, L. hardjo, and L. grippotyphosa . The first four serovars are most commonly isolated from dogs. In North America, the disease is perpetuated in domestic cows, horses and pigs and in wildlife that include mice, rats, raccoons, opossums, fox, skunk, deer, and woodchucks.

Transmission
Dogs become infected with leptospira through contact with the urine of infected animals. Stagnant water, contaminated with urine is a common source of infection as are rats. The organism can also be transmitted through mating, bites, and the consumption of infected carcasses. There are documented cases where transmission from parent to offspring occurred through the womb. Transmission is greatest during periods of wet weather.

Dynamics Of The Disease
Leptospira gain entrance to the bloodstream through mucous membranes or wounds. It takes 4-12 days for symptoms to occur. Once in the blood stream the organisms spread rapidly to body organs that include the liver, spleen and kidneys. The nervous system, genital tract and eyes also harbor leptospira. As the dog fights the disease by producing antibody, the organisms are cleared from most of the organs, remaining only in the kidneys from which they are shed for weeks or months in the urine. When death occurs it is often due to destruction of the liver (hepatitis). Liver necrosis is most common in dogs less than six months old. L. pomona and L. icterohaemorrhagiae have a predilection for the liver while L. canicola and L. grippotyphosa often spare the liver but colonize the kidneys. When people become infected , one third obtain the infection through contact with carrier dogs while another third contract the disease from contact with rats.

Symptoms of Leptospirosis
The first signs of leptospirosis are fever and depression. Dogs developing this disease are cold and shiver. They appear to ache and be tender all over. Soon they develop fevers of 103-104 degrees Fahrenheit. Joint pain and excessive bleeding sometimes occur. The dogs stop eating and drinking and often drool and vomit. Through vomission they loose fluids and become dehydrated. Dogs with fulminating infections soon become subnormal in temperature (hypothermia) and may die before signs of kidney and liver failure develop. In other dogs, infection of the kidneys leads to blood tinged reddish urine, oral ulcers and uremia. Inflammation of the covering of the brain (meningitis), inflammation of the iris and ciliary body of the eye (uveitis) and abortion have all been reported.

Dogs with more moderate cases of the disease soon drink water excessively. Their tenderness and reluctance to move is due to painful swollen kidneys. In those with liver involvement, the membranes that line the mouth and surround the eyes become yellowish (icteric, jaundiced). The majority of these dogs go on to recover in two or three weeks but a few permanently loose kidney function and die slowly from waste product overload (uremia). The dogs that recover can shed leptospira in their urine for months or even years. In these dogs the organism continues to live in the kidneys and reproductive organs.

Blood samples taken from dogs well into the disease process often show an elevated white blood cell count and a deficiency in thrombocytes which causes bleeding. Blood serum chemistry values often show kidney damage (elevated BUN and creatinine) and liver damage (elevated AST, ALT, Alkaline Phosphatase and bilirubin). Urine obtained from infected dogs may contain blood, protein and sugar reflecting damage to the kidney’s tubular filtering apparatus.

Diagnosis
Leptospirosis is diagnosed through test of the blood serum that measure the level of antibody present as well as the identity the strain of leptospira present. Fluorescent antibody tests or polymerase chain reaction tests identify the serovar responsible for causing the dog’s disease. The microscopic agglutination test or MAT is the most common test for antibody. It takes at least ten days for the dog to begin to produce antibody against the disease and several tests may be necessary to confirm the diagnosis. While a serum titer of 1:800 or more makes the disease highly likely a second test should be performed showing a rising titer in order to confirm that the infection is active. Recent leptospirosis vaccination can cloud the diagnosis. Occasionally, the bacteria can be isolated from the urine of infected dogs. A procedure called darkfield microscopy can identify leptospira in the urine sample. When the disease spreads to the dog’s owner the initial signs are fever, headaches, rash, myalgia and malaise.

Treatment
The first line of treatment of leptospirosis is to provide the dog with a suitable antibiotic. The penicillin class of antibiotics works well against leptospirosis (Penicillin G procaine 10,000-20,000 units/lb injected intramuscularly twice a day). After the acute phase of leptospirosis has passed, the drug of choice to prevent carrier states is doxycycline (1.5-2.5mg/lb twice a day orally). The newer fluoroquinolone antibiotics such as enrofloxacin and ciprofloxacin (2.5-10mg/lb/day) are also effective in treatment and elimination of carrier states. In addition to antibiotic therapy, medications are administered to stem vomiting and intravenous and subcutaneous fluids are give to correct dehydration. Dogs that die of the disease often do due to kidney failure. To prevent this, copious intravenous fluids help flush out the kidneys and prevent their destruction. When this is not sufficient and toxic waste products continue to build up in the dog’s body, hemodialysis has been effective in saving their lives.

Vaccination And Prevention
Limiting exposure to leptospira necessitates draining or fencing off sources of contaminated water. Vermin need to be eliminated from residential and rural areas. The best way to do this is to seal and protect all sources of feed that rodents and other vermin utilize.

The vaccines available for dogs are all killed extracts of leptospira. Most contain four of the nine serovars, L. canicola, L. icterohaemorrhagiae, L. grippotyphosa and L. pomona.
These bacterial extracts are usually marketed combined with living, attenuated (weakened) virus of canine distemper and parvovirus. When a vaccine reaction occurs in a dog, it is usually the leptospira extract or the antibiotic preservative that is the cause.

The leptospira portion of these vaccines produces six to eight months of immunity in dogs. Therefore, dogs kept in high exposure areas should be vaccinated twice yearly. I begin by vaccinating puppies at 9, 12 and 16 weeks of age. Leptospirosis vaccination is optional in house pets that are unlikely to be exposed to the disease.

No longer recommends that household urban dogs be vaccinated for leptospirosis. They give several reasons for this new recommendation:
1) The disease has become quite rare in the urban dog.
2) A more important reason is the frequency with which we see hives, facial swelling and even life-threatening vaccination reactions called anaphylaxis when we give vaccine “cocktails” that contain leptospirosis bacteria. The ”L” in DHLP, the most common vaccine cocktail, stands for leptospirosis. These reactions can be very mild or severe enough to cause death. These reactions do not occur on the initial vaccination but do increasingly on succeeding vaccinations.
3)Ththird reason is that the vaccines against leptospirosis are not that effective in preventing the disease and may actually facilitate carrier states.

Intestinal bacteria in dogs

After birth, gastrointestinal is colonised by various micro-organisms. The number of organisms increased from approximately 10²-10⁵ colony forming units (CFU) /ml in proximal small intestine to 10⁵-10⁹ CFU / mI in the distal small intestine, and then increased dramatically in the large intestine to approximately 10¹⁰-10¹¹CFU/ml in colon. This quantitative proximal-distal gradient is accompanied by complex qualitative changes from a predominantly aerobic flora in the small intestine to the large anaerobic flora in the large intestine. There is wide variation in the bacterial flora of normal individuals, and the concentration of May will be affected by various conditions including the environment, diet, scavenging and coprophagia. Increasing the number of bacteria in the small intestine carry an increase risk of damage the outcome. Whether this is a real clinical will depend on individual circumstances, including the composition of the diet that the bacteria can convert to potentially harmful metabolites. Nature of host response to the increased load may also be particularly important, and this May involve stimulation of immunoglobulin and mucus production, suppression of the potential damage to the cell mediated immune response, a compensatory production of structural and functional epithelial cell protein, and increased epithelial cell turnover. Threshold between the real normality and clinical disease in May therefore differ between individuals and is influenced by a complex balance between the microflora and the host. Clinical disease associated with bacterial overgrowth are common problems in dogs and occurs when this balance is tipped against the host.

Primary enteric bacterial pathogens can also cause acute clinical disease since they have the virulence factors that have Adverse effects on the gut. Adherence to the surface or invasion of the mucosa to facilitate long-term colonization by specific enteropathogens, predisposing to the carrier status or chronic disease, the result may depend on expression of virulence determine and host response.

Small intestinal bacterial

Small intestinal bacterial overgrowth (SIBO) is emerging as an important condition in dogs and emphasizes the potentially harmful effects of normal gut flora when the symbiotic relationship with the host is disrupted. This typically presents in young animals as chronic intermittent small bowel diarrhea, which in May accompanied by the loss of body weight or failure to gain weight. SIBO is ii a particular problem in many large breeds of dog, including German shepherd dogs Labradors and Golden retrievers, and colony dog appears to be particularly at risk.

The cause of bacterial

In most cases, it can not be identified, but a host of factors known to be a tendency for bacterial overgrowth, including disability gastric acid secretion, interference with normal motility or stasis, and disabled local immunity. The latter has been implicated in the German shepherd dog with 51,130, because this dog of a low serum and intestinal concentration of immunoglobulin A (Iga) that are important secreted protectant on the surface of the intestine. Other factors, stich as a potential stress or contaminated environment, diet and coprophagia, May also play a role and can contribute to the relatively high number of bacteria reported in kennelled dogs. Damaged as a result of overgrowth can involve competition by bacteria for calories and essential nutrients, production of harmful metabolites, and direct damage to the intestinal mucosa interfere with bowel function. Histological changes in gut biopsies from partial villus atrophy and lymphocyte / plasma cell infiltrate is present in 30% of cases, and in most cases, damage to the mucosa can not be seen by conventional light microscopy.

Diagnosis of bacterial

Diagnosis of SIBO in dogs is difficult and etirrently the assay of serum folate and cobalamin (B12) is the only practical screening test. An increased serum folate or reduced cobalamin concentration can provide indirect evidence of SIBO in dogs, and this has a reasonable specificity, although sensitivity is low. Increased sensitivity was achieved by hydrogen breath test following the oral administration of sugars. These sugars are metabolised by the bacteria present in the proximal small intestine in the SIBO resulted in the increase of breath hydrogen within 2 hours that do not occur in dogs with SIBO. Microbiological culture of duodenal juice obtained endoscopically or at laparotomy is needed to confirm the diagnosis of SIBO, and must show> 10⁵ colony formed units per ml. This is generally a mixture of flora, the most frequent isolates usually including enterococci and E. coli in dogs with aerobic overgrowth, and Clostridia in dogs with anaerobic overgrowth. Faecal culture does not help the diagnosis of overgrowth since the number and type of bacteria present in faeces are dominated by contributions from the large intestine.

Management of bacterial

Treatment with long-term oral broad spectrum antibiotics have proved to be effective, but there is a need for an alternative approach to the chronic management of dogs that relapse when antibiotics are withdrawn. Probiotics can theoretically help, but there are no objective studies that demonstrate efficacy as an approach. The management of SIBO with a low fat diet can help, because this can minimize the secretory diarrhea caused by bacterial metabolism of fatty acid and bile salt. Diet should also contain highly digestible carbohydrate and protein to minimize the availability of substrate for bacteria that will promote their life and can have other unpleasant consequences since intestinal gas is produced. A beneficial role for dietary fiber has not been documented, but it is clear that fiber-containing diets designed for weight reduction should not be used in these dogs that already have a compromised gut function as this could result in sufficient weight loss.

Pathogenic enteric Bacteria

Pathogenic stomach bacteria have colonization factors that encourage them live in the intestine and virulence factors that allow them to cause major intestinal disease. A number of potential enteropathogens were isolated from dogs, most especially Salmonella sp. and Canipylobacter sp. Their clinical importance is not yet fully defined, but clearly that some can cause clinical disease and may also represent zoonotic risk.

Colonization with stomach Pathogens

Pathogenic enteric bacteria are disseminated in the feces of infected animals and is most likely acquired by consuming contaminated food or water. Once access to the gastrointestinal tract has been achieved they then have to survive natural host defenses, including gastric acid, enzymes, mucus and local immunity. They also must compete with established non-pathogenic flora in order to ensure that they were standing on their predilection site. Colonization factors is therefore important component of pathogenicity and May include flagellae, chemotactins, mucinases, and fimbriae are hair-like projections that attach to specific receptors on the surface of the intestinal cells.

Virulence factors and clinical signs

Stomach bacteria cause clinical disease by many different mechanisms that may involve direct interaction with the intestinal mucosa and secretion of cytotoxins or enterotoxins. Various kinds of pathogenic E. coli, which is very popular in other species and emerge as important enteropathogens in dogs, illustrates the spectrum possible mechanisms. Invasive bacteria such as Salmonella sp., Campylobacter sp., Yersinia sp., Shigella sp. and enteroinvasive E. coli (EIEC) can invade the mucosa of the distal small intestine and colon causing acute enterocolitis. This is usually manifest as diarrhea accompanied by the passage of blood and mucus, and May lead to potentially fatal septicaemia if the organisms penetrate the intestinal barrier into the blood stream. Enteropathogenic E. coli (EPEC) also interacts directly with the mucosa of the small intestine, but cause more subtle damage than this professional invaders, resulting in a loss of microvilli from absorpsi epithelial cells in the small intestine. This compromises absorpsi function and causes the osmotic small bowel diarrhea.

Cytotoxins is secreted by a number of enteric pathogens including enterohaemorrhagic E. coli (EHEC), cytotoxic necrotising factor secreting E. coli and Clostridium perfringens. Cytotoxins is lethal to intestinal epithelial cells, causing bleeding and ulceration, potentially mimicking a severe enterocolitis caused by invasive bacteria. If EHEC to enter the circulation they can also damage endothelial cells and precipitate the haemolytic-uraemic syndrome. This mechanism has been responsible for the well-publicised human fatalities in Scotland and Japan following the food poisoning with the 0157 strain is usually derived from bovine products. In contrast to the cytotoxins, enterotoxins do not cause intestinal damage, but has a specific biochemical effect. They secreted eg by enterotoxigenic E. coli. (ETEC) and act as secretagogues resulted in a watery electrolyte-rich diarrhea. Many of these enteric pathogens cause acute clinical disease. However, properties such as adherence to the surface or invasion of the mucosa can promote long-term colonization by specific enteropathogens, predisposing to chronic disease or carrier status. The result may depend not only on the expression of virulence set but also on the host reaction, especially the ability to mount an effective immunological response.

Identification of stomach pathogens

Detection of enteropathogens in faecal samples initially involves conventional microbiological techniques, including biochemical characterisation and serotyping when appropriate. Identification of genes encoding virulence determine the new molecular approaches that proved invaluable, especially to distinguish between nonpathogenic E. coli. the main component normal intestinal flora, and different types of pathogenic E. coli of wolves in sheeps' clothing.

Main enteropathogens most frequently identified in dogs are Salmonella sp. and Campylobacter sp. This has been clearly associated with acute and chronic disease, usually causing haemorrhagic enterocolitis, but it can also be present in the clinical health service which potentially risks other animals and people. There is relatively little information on the prevalence of pathogenic E. coli. in dogs, although individual reports have isolated EPEC and ETEC from dogs with diarrhea. Our own studies have used gene probes to investigate E.coli. in faecal samples from dogs with diarrhea and clinical healthy dogs, all kept in the home environment. Results beginning shows that significantly more affected dogs were excreting pathogenic E. coli that hybridised with probes for EPEC and verocytotoxin. These findings support the possibility that pathogenic E. coli. can play a role in the pathogenesis of acute and chronic diarrhea in dogs. Additional preliminary studies of kennelled dogs suggest their May act as a carrier of pathogenic E. coli that can be transmitted and cause clinical disease in susceptible individuals. Vulnerability can involve environmental factors such as stress, but also an innate inability to mount an effective mucosal immune response to this organism.

Treatment and prevention of infection

Treatment acute cases, depending on the severity of clinical signs. Mild cases require little or no treatment, whereas parenteral antibiotics and intensive fluid therapy is indicated in severe cases, especially when there is evidence of septicaemia or endotoxaemia. Chronic cases can he difficult to manage and this may be due to a number of factors including poor support from the down host response, antibiotic resistance, the failure of antibiotics to reach invasive enteropathogens, or Reinfection from the environment.

There are obviously a force the argument for the administration of antibiotics in severe cases, but their use is controversial, especially in the clinically-healthy carriers. Options May be guided by antibiotic sensitivity testing, but generally antibiotic selection for clinical disease and to eliminate carrier status is enrofloxacin for salmonellosis and erythromycin for campylobacteriosis. Clearly, attention should also he given to the identification of sources of infection and the introduction of effective management procedures to prevent infection, especially if the dogs are housed together in the community. In an assessment 7oonotic potential it is relevant to consider that approximately 100,000 salmonella, but as few as 500 campylohacter organisms may be needed to cause clinical disease. The zoonotic implications of pathogenic E. coli infection in dogs is not well understood, but the infected animals should be considered a potential risk to relevant information to the contrary is available.

Canine parvovirus

Canine parvovirus (type 2) is a contagious virus mainly affecting dogs. The disease is highly infectious and is spread from dog to dog by direct or indirect contact with their feces. It can be especially severe in puppies that are not protected by maternal antibodies vaccination. It has two distinct presentations, a cardiac and intestinal form. The common signs of the intestinal form are severe vomiting and severe haemorrhagic (bloody) diarrhea. The cardiac form causes respiratory or cardiovascular failure in young puppies. Treatment often involves veterinary hospitalization. Vaccines can prevent this infection, but mortality can reach 91% in untreated cases.

There are two types of canine parvovirus called canine parvovirus type 1 CPV1) and canine parvovirus type 2 (CPV2). CPV2 causes the most serious disease and affects domesticated dogs and wild canids. There are variants of CPV2 called CPV-2a, CPV-2b and CPV-2c. Types 2a and 2b are distinct from the original CPV type 2 in terms of virulence and their ability to infect and cause disease in cats too. CPV-2c is a newly identified variant similar to 2b. The viral protein of 2c contains one amino acid different from CPV-2b but it is believed this could be significant. 2c strains have been identified in parts of Europe, the Americas and in Asia. Emergence of this strain has led to claims of ineffective vaccination of dogs, however studies have shown that the existing CPV vaccines still provide adequate levels of protection against CPV type 2c.

Prevention and decontamination

Prevention is the only way to ensure that a puppy or dog remains healthy since the disease is extremely virulent and contigious. The virus is extremely hardy and has been found to survive in feces and other organic material such as soil for over a year. It survives extremely cold and hot temperatures. The only household disinfectant that kills the virus is bleach.

Weaning puppies can be vaccinated with a modified live virus low passage high titer vaccine at 6 weeks of age, then every 3 to 4 weeks until 15 or 16 weeks. Puppies are initially protected through passive immunity derived from the mother. These maternal antibodies wear off before the puppy's immune system is mature enough to fight off CPV2 infection. Maternal antibodies also interfere with vaccination for CPV2 and can cause vaccine failure. Thus puppies are generally vaccinated in a series of shots, extending from the earliest time that the immunity derived from the mother wears off until after that passive immunity is definitely gone. Older puppies (16 weeks or older) are given 3 vaccinations 3 to 4 weeks apart. The duration of immunity of vaccines for CPV2 has been tested for all major vaccine manufacturers in the United States and has been found to be at least three years after the initial puppy series and a booster 1 year later.

A dog that successfully recovers from CPV2 sheds virus for a few days. Ongoing infection risk is primarily from faecal contamination of the environment due to the virus's ability to survive many months in the environment. Neighbours and family members with dogs should be notified of infected animals so that they can ensure that their dogs are vaccinated or tested for immunity. Vaccine will take up to 2 weeks to reach effective levels of immunity, the contagious individual should remain in quarantine until other animals are protected.

Treatment

Survival rate depends on how quickly CPV is diagnosed, the age of the animal and how aggressive the treatment is. Treatment for severe cases that are not caught early usually involves extensive hospitalization, due to the severe dehydration and damage to the intestines and bone marrow. A CPV test should be given as early as possible if CPV is suspected in order to begin early treatment and increase survival rate if the disease is found.

Treatment ideally consists of crystalloid IV fluids and/or colloids, antinausea injections (antiemetics) such as metoclopramide, dolasetron, ondansentron, and prochlorperazine, and antibiotic injections such as cefoxitin, metronidazole, timentin, or enrofloxacin. IV fluids are administered and antinausea and antibiotic injections are given subcutaneously, intramuscularly, or intravenously. The fluids are typically a mix of a sterile, balanced electrolyte solution, with an appropriate amount of B-complex vitamins, dextrose and potassium chloride. Analgesic medications such as buprenorphine are also used to counteract the intestinal discomfort caused by frequent bouts of diarrhea.

In addition to fluids given to achieve adequate rehydration, each time the puppy vomits or has diarrhea in a significant quantity, an equal amount of fluid is administered intravenously. The fluid requirements of a patient are determined by their body weight, weight changes over time, degree of dehydration at presentation and surface area. The hydration status is originally determined by assessment of clinical factors like tacky mucous membranes, concentration of the urine, sunken eyes, poor skin elasticity and bloodtests.

A blood plasmatransfusion from a donor dog that has already survived CPV is sometimes used to provide passive immunity to the sick dog. Some veterinarians keep these dogs on site, or have frozen serum available. There have been no controlled studies regarding this treatment. Additionally, fresh frozen plasma and human albumin transfusions can help replace the extreme protein losses seen in severe cases and help assure adequate tissue healing.

Once the dog can keep fluids down, the IV fluids are gradually discontinued, and very bland food slowly introduced. Oral antibiotics are administered for a number of days depending on the white blood cell count and the patient's ability to fight off secondary infection. A puppy with minimal symptoms can recover in 2 or 3 days if the IV fluids are begun as soon as symptoms are noticed and the CPV test confirms the diagnosis. However, even with hospitalization, there is no guarantee that the dog will be cured and survive.

Unconventional treatments
There is no specific antiviral treatment for CPV. However, there have been anecdotal reports of oseltamivir (Tamiflu) reducing disease severity and hospitalization time in canine parvovirus infection. The drug may limit the ability of the virus to invade the crypt cells of the small intestine and decrease gastrointestinal bacteria colonization and toxin production. There is also anecdotal evidence suggesting that colloidal silver is effective at treating CPV although currently regulatory authorities are discouraging its use due to potential toxicity issues and lack of demonstrated efficacy. Lastly, recombinant feline interferon omega (rFeIFN-ω), produced in silkworm larvae using a baculovirus vector, has been demonstrated by multiple studies to be an effective treatment.

Canine distemper

Canine distemper is a very serious viral disease affecting animals in the families Canidae, Mustelidae, Mephitidae, Hyaenidae, Airulidae, Procyonidae, Pinnipedae, some Viverridae and Ffelidae (though not domestic catsl; 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 Engglish 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.

History

Although 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

Puppies 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, enchepalitis 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 enchepalitis are more common. In older dogs that do develop distemper enchephalomyelitis, 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 meningoencephalomyelitis.

Gastrointestinal and respiratory symptoms

Commonly 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 Symptoms

The 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.” As the condition progresses, the seizures worsen and the dog may fall to its side, exhibiting grand mal convulsions. 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 that survive usually have a small tic or twitch of varying levels of severity. With time this tic will usually diminish.

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.

Treatment and prevention

There is no specific treatment for canine distemper. The dog should be treated by a veterinarian, usually with antibiotics for secondary bacterial infections, intravenous fluids, and nutritional supplements. The prognosis is poor. In, vitro, ribavirin, an antiviral effective in treating measles and other viruses, has also shown effective against Canine distemper virus by means of error catastrophe. More research is now needed in vivo.

There exist a number of vaccines against canine distemper for dogs and domestic ferrets, 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 virus. 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.

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. 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

Bacterial infections in dogs

Brucellosis

Brucellosis, also called undulant fever, or Malta fever, is a highly contagious zoonosis caused by ingestion of unsterilized milk or meat from infected animals, or close contact with their secretions. Brucella spp. are small, gram negative, non-motile, non-spore-forming rods, which function as facultative intracellular parasites that cause chronic disease, which usually persists for life. Brucellosis has been recognized in both animals and humans since the 19th century.

History and nomenclature

The disease now called brucellosis, under the name "Mediterranean fever", first came to the attention of British medical officers in Malta during the CrimeanWar in the 1850s. The causal relationship between organism and disease was first established by Dr. David Bruce in 1887.

In 1897 Danish Veterinarian Bernhard Bang isolated Brucella abortus as the agent and the additional name Bang's disease was assigned. In modern usage "Bang's disease" is often shortened to just "bangs" when ranchers discuss the disease or vaccine.

Maltese doctor and archaeologist Sir Temi Zammit identified unpasteurized milk as the major source of the pathogen in 1905, and it has since become known as Malta Fever, or deni rqiq locally. In cattle this disease is also known as contagious abortion and infectious abortion.

The popular name "undulant fever" originates from the characteristic undulance (or "wave-like" nature) of the fever which rises and falls over weeks in untreated patients. In the 20th Century, this name, along with "brucellosis" (after Brucella, named for Dr Bruce), gradually replaced the 19th Century names "Mediterranean fever" and "Malta fever".

In 1989, Saudi Arabian neurologists discovered neurobrucellosis, a neurological involvement in brucellosis.

Brucellosis in animals

Species infecting domestic livestock are B. melitensis (goats and sheep), B. suis (pigs, see Swine brucellosis), B. abortus (cattle and bison), B. ovis (sheep), and B. canis (dogs). B. abortus also infects bison and elk in North America and B. suis is endemic in caribou. Brucella species have also been isolated from several marine mammal species (pinnipeds and cetaceans.)

The causative agent of brucellosis in dogs is Brucella canis. It is transmitted to other dogs through breeding and contact with aborted fetuses. Brucellosis can occur in humans that come in contact with infected aborted tissue or semen. The bacteria in dogs normally infect the genitals and lymphatic system, but can also spread to the eye, kidney, and intervertebral causing discospondylitis). Symptoms of brucellosis in dogs include abortion in female dogs and scrotal inflammation and orchitis (inflammation of the testicles) in males. Fever is uncommon. Infection of the eye can cause uvitis, and infection of the intervertebral disc can cause pain or weakness. Blood testing of the dogs prior to breeding can prevent the spread of this disease. It is treated with antibiotics as with humans, but it is difficult to cure.

Diagnosis of brucellosis relies on:

1. Demonstration of the agent: blood cultures in tryptose broth, bone marrow cultures. The growth of brucellae is extremely slow (they can take until 2 months to grow) and the culture poses a risk to laboratory personnel due to high infectivity of brucellae.
2. Demonstration of antibodies against the agent either with the classic Huddleson, Wright and/or Bengal Rose reactions, either with ELISA or the 2-mercaptoethanol assay for IgM antibodies associated with chronic disease
3. Histologic evidence of granulomatous hepatitis (hepatic biopsy)
4. Radiologic alterations in infected vertebrae : the Pedro Pons sign (preferential erosion of antero-superior corner of lumbar vertebrae) and marked osteophytosis are suspicious of brucellic spondylitis.

The disease's sequelae are highly variable and may include granulomatous hepatitis, arthritis, spondylitis, anemia, leukopenia,thrombocytopenia, meningitis, uvitis, neuritis and endocarditis.

Treatment and prevention

Antibiotic like tetracyclins, rifampicin and the aminoglykosides streptomycin and gentamycin are effective against Brucella bacteria. However, the use of more than one antibiotic is needed for several weeks, because the bacteria incubates within cells.

The gold standard treatment for adults is daily intramuscular injections of streptomycin 1 g for 14 days and oral doxycycline 100 mg twice daily for 45 days (concurrently). Gentamicin 5 mg/kg by intramuscular injection once daily for 7 days is an acceptable substitute when streptomycin is not available or difficult to obtain. Another widely used regimen is doxycycline plus rifampin twice daily for at least 6 weeks. This regimen has the advantage of oral administration. A triple therapy of doxycycline, together with rifampin and cotrimoxazole has been used successfully to treat neurobrucellosis. Doxycycline is able to cross the blood-brain barrier, but requires the addition of two other drugs to prevent relapse. Ciprofloxacin and co-trimoxazole therapy is associated with an unacceptably high rate of relapse. In brucellic endocarditis surgery is required for an optimal outcome. Even with optimal antibrucellic therapy relapses still occur in 5-10 percent of patients with Malta fever. The main way of preventing brucellosis is by using fastidious hygiene in producing raw milk products, or by pasteurization of all milk that is to be ingested by human beings, either in its pure form or as a derivate, such as cheeese. Experiments have shown that cotrimoxyzol and rifampin are both safe drugs to use in treatment of pregnant women who have Brucellosis.

Biological warfare

In 1954, B. suis became the first agent weaponized by the United States at its Pine Bluff Arsenall in Arkansas. Brucella species survive well in aerosols and resist drying. Brucella and all other remaining biological weapons in the U.S. arsenal were destroyed in 1971-72 when the U.S. offensive biological weapons (BW) program was discontinued.

Viral disease in dogs

• Rabies
  
  
  Rabies is a deadly disease caused by a virus that attacks the nervous system. The virus is secreted in saliva and is usually transmitted to people and animals by a bite from an infected animal. Less commonly, rabies can be transmitted when saliva from a rabid animal comes in contact with an open cut on the skin or the eyes, nose, or mouth of a person or animal. Once the outward signs of the disease appear, rabies is nearly always fatal.

  
  
  Rabies is a viral disease that causes acute encephalitis in animals and man. Only mammals can get rabies; birds, fish, reptiles and amphibians do not. Most cases of rabies occur in wild animals - mainly skunks, raccoons, bats, and foxes. In recent years, cats have become the most common domestic animal infected with rabies. This is because many cat owners do not vaccinate their cats before the cats are exposed to rabid wildlife outdoors. Rabies also occurs in dogs and cattle in significant numbers and, while not as common, has been diagnosed in horses, goats, sheep, swine and ferrets.
  Improved vaccination programs and control of stray animals have been effective in preventing rabies in most pets. Approved rabies vaccines are available for cats, dogs, ferrets, horses, cattle and sheep. Licensed oral vaccines have been used for mass immunization of wildlife.
  Once the rabies virus enters the body, it travels along the nerves to the brain. Dogs, cats, and ferrets with rabies may show a variety of signs, including fearfulness, aggression, excessive drooling, difficulty swallowing, staggering, and seizures. Rabid wild animals may only display unusual behavior; for example, an animal that is usually only seen at night may be seen wandering in the daytime. In addition to those signs seen in dogs and cats, horses, cattle, sheep, and goats with rabies may exhibit depression, self mutilation, or increased sensitivity to light. Rabies vaccination and animal control programs, along with better treatment for people who have been bitten, have dramatically reduced the number of human cases of rabies in the United States. Most of the relatively few, recent human cases in this country have resulted from exposures to bats. A few rabies cases have resulted from corneal or organ/tissue transplants from an infected donor, but these have been extremely rare. Dogs are still a significant source of rabies in other countries, so travelers should be aware of this risk when traveling outside of the United States.

Control Rabies

1. Have your veterinarian vaccinate your dogs, cats, ferrets, and select horses and livestock. Your veterinarian will advise you on the recommended or required frequency of vaccination in your area.
2. Reduce the possibility of exposure to rabies by not letting your pets roam free. Keep cats and ferrets indoors, and supervise dogs when they are outside. Spaying or neutering your pet may decrease roaming tendencies and will prevent them from contributing to the birth of unwanted animals.
   
3. Don't leave exposed garbage or pet food outside, as it may attract wild or stray animals.
   
4. Wild animals should never be kept as pets. Not only may this be illegal, but wild animals pose a potential rabies threat to caretakers and to others.
   
5. Observe all wild animals from a distance. A rabid wild animal may appear tame but don't go near it. Teach children NEVER to handle unfamiliar animals — even if they appear friendly.
   
6. If you see a wild animal acting strangely, report it to the city or county animal control department.

If have bitten

1. Don’t panic, but don’t ignore the bite. Wash the wound thoroughly and vigorously with soap and lots of water.
   
2. Call your physician immediately and explain how you were bitten. Follow the doctor’s advice. If necessary, your physician will give you the post exposure treatment recommended by the United States Public Health Service and may also treat you for other possible infections that could result from the bite.
3. If possible, confine or capture the animal under a large box or other container if that can be done safely. Once captured, don’t try to pick up the animal. Call the local animal controlauthorities to collect it. If the animal cannot be captured, try to memorize its appearance (size, color, etc.) and where it went after biting you.
4. If it is a wild animal, only try to capture it if you can do so without getting bitten again. If the animal cannot be contained and must be killed to prevent its escape, do so without damaging the head. The brain will be needed to test for rabies.
5. Report the bite to the local health department. Prompt and appropriate treatment after being bitten and before the disease develops can stop the infection and prevent the disease.

Dog Breed

Dog breeds are groups of closely related and visibly similar domestic dogs, which are all of the subspecies Canis lupus familiaris, having characteristic traits that are selected and maintained by humans, bred from a known foundation stock.

The term dog breed may also be used to refer to natural breeds or landraces, which arose through time in response to a particular environment which included humans, with little or no selective breeding by humans. Such breeds are undocumented, and are identified by their appearance and often by a style of working. Ancient dog breeds are some of the modern (documented) descendants of such natural breeds.

A dog breed is represented by a sufficient number of individuals to stably transfer its specific characteristics over generations. Dogs of same breed have similar characteristics of appearance and behavior, primarily because they come from a select set of ancestors who had the same characteristics. Dogs of a specific breed breed true, producing young closely similar to the parents. An individual dog is identified as a member of a breed through proof of ancestry, using genetic analysis or written records of ancestry. Without such proof, identification of a specific breed is not reliable. Such records, called stud books, may be maintained by individuals, clubs, or other organizations.

In biology, subspecies, race and breed are equivalent terms. Breed is usually applied to domestic animals; species and subspecies, to wild animals and to plants; and race, to humans. Colloqiual use of the term Dog breed, however, does not conform to scientific standards of taxonomic classification. Breeds do meet the criteria for subspecies: an interbreeding group of individuals who pass on characteristic traits and would likely merge back into a single homogeneous group if external barriers were removed. The recognition of distinct dog breeds is not maintained by a scientific organization; they are maintained by a number of independent kennel clubs that need not apply to scientific standards and are often inconsistent. For instance, the Belgian Shepherd Dog is separated into four distinct breeds by some clubs, but not in others. Further, some groups of dogs which clearly share a persistent set of characteristics and documented descent from a known foundation stock may still not be recognized by some clubs as breeds. For instance, the feist is a hunting dog raised in the Southern United States for hunting small game. Feists have a consistent set of characteristics that reliably discriminate them from other dog type and breeds. However, the United Kennel Club recognizes one breed of feist, the Treeing Feist, but the American Kennel Club, does not recognize any feist breed.

A dog is said to be Purebred if its parents were purebred and it meets the standards of the breed. Purebred dog breeders of today "have inherited a breeding paradigm that is, at the very least, a bit anachronistic in light of modern genetic knowledge, and that first arose out of a pretty blatant misinterpretation of Darwin and an enthusiasm for social theories that have long been discredited as scientifically insupportable and morally questionable." Moral questions regarding purity of breed include obligatory surgical procedures to spay or neuter animals in numerous contexts. The American Kennel Club, for instance, allows mixed-breed dogs to be shown but requires these animals to be altered. It does not make such requirements for purebred dogs. California Assembly Act AB 1634 was a bill introduced in 2007 that would require all non-working dogs of mixed-breed over the age of 6 months to be neutered or spayed. The bill was morally controversial, leading the American Kennel Club to fight the bill.

The clear genetic distinction between breeds of dog has made dogs of specific breeds good subjects for genetic and human medical research. "Using the dog as a discovery tool" in studying how cancer affects specific breeds may lead to identifying "susceptibility genes that have proved intractable in human families and populations."