Canine Salmonellosis | Salmonellosis in Dogs
There are numerous Salmonella serotypes that may cause disease. The bacteria may originate from animals shedding the organism (e.g., infected dogs and cats) or from contaminated foods (especially poultry and eggs).

Salmonella spp. are seldom confirmed to cause dogs or cats GI disease, even though the bacteria are often present in the colon and/or mesenteric lymp nodes. Salmonella spp. may produce acute or chronic diarrhea, septicemia, and/or sudden death, especially in very young dogs and cats. Salmonellosis in dogs and cats can produce a syndrome that closely mimics parvoviral enteritis. The fact that samonellosis occasionally develops during or after canine parvoviral enteritis makes the situation more confusing.

Culture of Salmonella spp. from the blood confirms septicemia. Diagnosis of GI salmonellosis requires culture of the organism from the feces or mucosa, appropriate clinical signs, elimination of other causes (e.g., parvovirus), and response to therapy. However, Salmonella may be cultures from normal dogs and cats; therefore, definitive diagnosis can be difficult. Successful fecal culture often necessitates use of enrichment and/or selective media. Identification by polymerase chain reaction (PCR) can be a sensitive method of diagnosis.

If salmonellosis in dogs and cats is diagnosed, treatment depends on the animal's clinical signs. Septicemic animals should receive supportive therapy and parental antibiotics as determined by susceptibility testing, but quinolones, potentiated sulfa drugs, and chloramphenicol are often good initial choices.

Dogs and cats with diarrhea may need only supportive therapy; antibiotics are a dubious value and might promote a carrier state. Infected animals might be public health risks and should be isolated from other animals, at least until they are asymptomatic. even when signs disappear, reculturing of feces is reasonable to ensure that shedding has stopped. Individuals in contact with the animals, its environment, and its waste should wear protective clothing and wash with disinfectants such as phenolic compounds and bleach.

The prognosis is usually good in dogs and cats with only diarrhea but guarded in septicemic animals.

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Canine Salmon Poisoning | Salmon Poisoning in Dogs

Salmon poisoning in dogs is caused by Neorickettsia helminthoeca. Dogs are infected when they eat fish (primarily salmon) infected with a fluke (Nanophyetus salmincola) that carries the rickettsia. The rickettsia spreads to the intestines and most lymph nodes, causing inflammation. The disease is principally found in the Pacific northwestern Unites States because the snail intermediate host for N. salmincola lives there.

Dogs, not cats, are affected. The severity of signs varies and may include fever, anorexia, vomiting, generalized lymphadenopathy and diarrhea. The diarrhea is typically small bowel but may become bloody. Inappropriate therapy may result to death.

Presumptive diagnosis is usually based on the dog's habitat plus a history of recent consumption of raw fish or exposure to streams or lakes. Finding Nanophyetus spp. ova in the stool or rickettsia in fine-needles aspirates of enlarged lymph nodes is confirmatory.

Salmon poisoning treatment for dogs consists of symptomatic control of dehydration, vomiting, and diarrhea and elimination of the rickettsia and fluke. Tetracycline, oxy tetracycline, doxycyline, or chloramphenicol eliminates the rickettsia. The fluke is killed with praziquantel.

The prognosis depends on the clinical severity at the time of diagnosis. Most dogs respond favorably to tetracyclines and supportive therapy. The key to success is awareness of the disease. Untreated salmon poisoning in dogs has a poor prognosis.

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Canine Coronaviral Enteritis | Coronaviral Enteritis in Dogs

Coronaviral enteritis in dogs occurs when coronavirus invades and destroys mature cells on the intestinal villi. Because intestinal crypts remain intact, villi regenerate faster in dogs with coronaviral enteritis than in dogs with parvoviral enteritis; bone marrow cells are not affected.
Coronaviral enteritis in dogs is typically less severe than classic parvoviral enteritis and rarely causes hemmorrhagic diarrhea, septicema, or death. Older dogs may be affected in addition to younger dogs. Signs may last approximately 3 to 20 days, and small or very young dogs may die from dehydration or electrolyte abnormalities if they are not properly treated. Dual infection with parvovirus may produce a high incidence of morbidity and mortality.

Because coronaviral enteritis in dogs is usually much less severe than many other enteritides, it is seldom definitely diagnosed. Most dogs are treated symptomatically for acute enteritis until they improve. Electron microscopic examination of feces obtained early in the course of the disease can be diagnostic. However, the virus is fragile and easily disrupted by inappropriate handling of the feces. A history of contagion and eliminating other causes are reasons to suspect coronaviral enteritis in dogs.

Fluid therapy, motility modifiers and time should resolve most cases of coronaviral enteritis in dogs. Symptomatic therapy is usually successful except perhaps for very young dogs. A vaccination is available but of uncertain value except perhaps in dogs at high risk of infection (e.g., those in infected kennels or dog shows). The prognosis for recovery is usually good.

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Dog dehydration symptoms and signs

Dehydrated dogs are treated by replacing the estimated fluid deficit. First, the degree of dehydration in dogs must be estimated. Prolonged skin tenting is usually the first noticed dehydration symptom indogs at 5% to 6%. Dry, tacky oral mucous membranes usually indicate 6% to 7% dehydration.

Next, multiplication of the estimated percentage of dehydration by the dog's weight (in kg) yields the number of liters needed to replace the deficit. This amount is replaced over 2 to 8 hours, depending on the dog's condition. The fluid rate generally should not exceed 88 ml/kg/hr. It is better to overestimate rather than underestimate the fluid deficit, unless the dog has congestive heart failure, anuric or oliguric renal failure, severe hypoproteinemia, severe anemia, or pulmonary edema.

Maintenance fluids are administered once fluid deficits have been replaced. Maintenance requirements are approximately 60 ml/kg/day. In general, potassium should be supplemented if the dog is anorexic or vomiting, has diarrhea, or is receiving prolonged or intensive fluid therapy. Adequacy of fluid therapy can be gauged by regularly weighing the dog. Progressive weight loss implies inadequate fluid therapy in the face of ongoing fluid loss. A cjange of 1 pound represents approximately 500 ml of water. Ongoing losses can be estimated from observation of vomiting, diarrhea and urination, however, underestimation is common.

Development of inspiratory pulmonary crackles, a systolic heart murmur, a gallop rhythm, or edema (especially cervical) suggests overhydration. Central venous pressure is an excellent indicator of excessive fluid administration, however, it is rarely needed except in dogs with severe cardiac or renal failure and those receiving aggressive fluid therapy.
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Hypoallergenic dog food and elimination diets are indicated if a dietary allergy (i.e., an immune-mediated hypersensitivity to a dietary component) or intolerance (i.e., a non-immune-mediated problem) is suspected, respectively. Both type of diets will henceforth be referred to as hypoallergenic dog food.

These diets may be composed of the same ingredients found in bland diets; however, they must be formulated so that the dog is fed food that it either has not eaten before (and hence could not be responsible for causing allergy or intolerance) or that is very unlikely to provoke allergy or intolerance (e.g., potatoes). Commercial elimination diets are available; however, it may be best to first try a homemade one if the owners are willing to prepare it.

Hypoallergenic dog food diets must be used for at least 6-8 weeks before their efficacy can accurately be determined. It is critical that no other foods or treats be give to the dog during this time; this include pills, toys, and medications with flavoring. If the signs resolve during this time, hypoallergenic dog food should be continued for at least 4 to 6 more weeks to ensure that it is the diet that is responsible and not a spontaneous fluctuation of the disease. If hypoallergenic dog food seems effective, a more convenient commercial diet may then be substituted for the homemade one. If the homemade diet is to be continued, appropriate vitamins, minerals and fatty acids should be added to balance it.

Dogs and cats stomatitis causes, symptoms and treatment

There are many causes of canine and feline stomatitis. The common causes are: renal failure, trauma (foreign objects, chewing or ingesting caustic agents, chewing on electrical cords), Immune-mediated disease (pemphigus, lupus), upper respiratory viruses (feline viral rhinotracheitis, feline calocivirus), infection secondary to immunosuppression (feline leukemia virus, feline immunodeficiency virus), tooth root abscesses, severe periodontitis, osteomyelitis and thallium intoxication. The clinician should always consider the possibility of immunosuppression with secondary stomatitis in dogs and cats (e.g., diabetes mellitus, hyperadrenocorticism).

Most dogs and cats with stomatitis have thick, ropey saliva, severe halitosis, and/or anorexia caused by pain. Some animals are febrile and lose weight. A thorough oral examination usually requires that the animal be under anesthesia. Stomatitis in dogs and cats is diagnosed by gross observation of the lesions, but an underlying cause should be sought. Biopsy is routinely indicated, as are routine clinical pathology data and radiographs of the mandible and maxilla, including the tooth roots.

Stomatitis treatment in dogs and cats is both symptomatic (to control signs) and specific (e.g., directed at the underlying cause). Teeth cleaning and aggressive antibacterial therapy (i.e., systemic antibiotics effective against aerobes and anaerobes, cleansing oral rinses with antibacterial solutions such as chlohexidine) often help. In some animals, extracting teeth that are associated with the most severely affected areas may help. Bovine lactoferrin has been reported to ameliorate otherwise resistant lesions in cats. The prognosis depends on the underlying cause.

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In dogs and cats with gastrointestinal problems, antibiotics are primarily indicated if aspiration pneumonia, fever, a leukogram suggestive of sepsis, severe neutropenia, antibiotic-responsive enteropathy, clostridial colitis, symptomatic Helicobacter gastritis, or perhaps hematemesis or melena is found or suspected. Animals with an acute abdomen may reasonably be treated with antibiotics while the nature of the disease is being defined. However, most animals with enteritis or gastritis of unknown cause do not benefit from antibiotic therapy. In general, the routine use of antimicrobials with alimentary tract disorders is not recommended, unless the animal is at high risk for infection or a specific disorder is being treated.

Nonabsorbable aminoglycosides (e.g., neomycin) are often used to "sterilize" the intestines. However, they do not kill anaerobic bacteria, which are the predominant type found there. Further, there are a plethora of viral and dietary causes of acute enteritis that are not responsive to antibiotics. Thus, aminoglycosides given PO are not indicated unless a specific infection (e.g., campylobacteriosis) is being considered. Some data suggest that neomycin is effective against Giardia.

Broad-spectrum antibiotics effective against anaerobes (e.g., tetracycline) may be used for the treatment of antibiotic-responsive enteropathy. Metronidazole may also be used for this purpose. Inappropriate therapy with some of these drugs may hypothetically eliminate enough resident bacteria that overgrowth of pathogenic bacteria in the colon occurs. However, this is rarely a clinical problem in dogs and cats. One should treat for at least two weeks before deciding that therapy has been unsuccessful.

Occasionally, dogs and cats have enteritis caused by a specific bacterium. However, even this is not necessarily an indication for antibiotics. Clinical signs resulting from one bacterial enteritides (e.g., salmonellosis, enterohemorrhagic Escherichia .coli) generally do not resolve more quickly when the animal is treated with antibiotics, even those to which the bacteria are sensitive. Dogs and cats with viral enteritis but without obvious systemic sepsis may reasonably be treated with antibiotics if secondary sepsis is likely to occur (e.g., those with neutropenia or severe hemorrhagic diarrhea). First-generation cephalosporins (e.g., cephazolin) are often effective for such use. We also recommend this natural balanced real-meat dog food and natural dietary supplement for recovery.

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Dysautonomia in dogs and cats is an idiopathic condition that causes loss of automatic nervous system functions. Clinical signs vary substantially. Megaesophagus and subsequent regurgitation are common (not invariable); however, dysuria and a distended urinary bladder, mydriasis, and lack of pupillary light response, dry mucus membranes, weight loss, constipation, vomiting, and anorexia are reported. There appear to be geographic areas (e.g., Missouri and surrounding states), that currently have an increased incidence of the disease for some reason.

Dysautonomia in dogs and cats is usually suspected clinically by finding dysuria, dry mucus membranes, and abnormal pupillary responses. Radiographs revealing distention of multiple areas of the alimentary tract (e.g., esophagus, stomach, small intestine) also are suggestive. A presumptive, antemortem diagnosis is usually made by observing the effects of pilocarpine on pupil size after 1 to 2 drops of 0.05% pilocarpine are placed in one eye only. Finding that the treated eye rapidly constricts whereas the untreated eye does not is consistent with dysautonomia in dogs and cats.

Similarly, finding that a dysuric dog with a large urinary bladder can urinate after administration of 0.04 mg bethanechol/kg SQ is also suggestive (although not all affected animals respond). Definitive diagnosis requires histopathology of autonomic ganglia, which can only be obtained at necropsy.

Treatment is palliative. Bethanechol can be given (1.25 to 5 mg daily) to aid in urinary evacuation. The urinary bladder should be expressed as needed. Gastric prokinetics (e.g., cisapride) may help lessen vomiting. Antibiotics may be administered for aspiration pneumonia secondary to megaesophagus.

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Cats dental health care.

Bacterial proliferation and toxin production, usually associated with tartar buildup, destroy normal gingival structures and produce inflammation. Immunosuppression due to feline leukemia virus (FeLV) and feline immunodeficiency virus (FIV) can predispose some cats to this disease. Many clinical features are asymptomatic, but halitosis, oral discomfort, refusal to eat, dysphagia, drooling and tooth loss may occur.

Visual examination of the gums reveal hyperemia around the tooth margins. Gingival recession may reveal tooth roots. Supragingival and subgingival tartar should be removed, and the crowns should be polished. Antimicrobial drugs effective against anaerobic bacteria (e.g., amoxicillin, clindamycin, metronidazole) may be used before and after cleaning teeth. Regular brushing of the teeth and/or oral rinsing with a veterinary chlorexidine solution formulated for that purpose helps to prevent recurrence. The prognosis is good with proper therapy.

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Tumors of the oral cavity in cats are less common than in dogs, but they are usually squamous cell carcinomas, which are diagnosed and treated as described for dogs. However, eosinophilic granulomas (which have a much better prognosis) are relatively common in cats and can closely mimic carcinoma. Dysphagia, halitosis, anorexia, and/or bleeding are common features of these tumors.

A large, deep biopsy is needed because it is crucial to differentiate malignant tumors from eosinophilic granulomas. The superficial aspect of many masses of the oral cavity in cats is ulcerated and necrotic as a result of the proliferation of normal oral bacterial flora, making it difficult to interpret this part of the mass.

Surgical excision is desirable as treatment. Radiation therapy and/or chemotherapy may benefit cats with incompletely excised squamous cell carcinomas not involving the tongue or tonsil. In general, the prognosis for cats with tumors of the tongue or tonsil is guarded to poor.

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In dogs, most soft tissue masses of the oral cavity are neoplasms, and most of these are malignant (i.e., melanoma, squamous cell carcinomas, fibrosarcoma). However, acanthomatous epulides, fibromatous epulides, (classically in Boxers), oral papillomatosis, and eosinophilic granulomas also occur.

The most common signs of tumors of the oral cavity in dogs are halitosis, dysphagia, bleeding, or a growth protruding from the mouth. Papillomatosis and fibromatous periodontal hyperplasia are benign growths that may cause discomfort when eating and occasionally cause bleeding, mild halitosis, or tissue protrusion from the mouth.

An examination of the oral cavity (which may require that the dog is under anesthesia) usually reveals a mass involving the gingiva, although the tonsillar area, hard palate, and tongue can also be affected. Diagnosis require cytologic or histopathologic analysis, although papillomatosis and epulis may be strongly suspected from their gross appearance. The preferred diagnostic approach in a dog with a mass of the oral cavity is to perform an incisional biopsy and to obtain thoracic and skull radiographs of the affected area.

If malignancy is a diagnostic consideration, thoracic radiographs should be obtained to evaluate for metastases (seldom seen but a very poor prognostic sign if present), and maxillary and mandibular radiographs should be obtained to check for bony involvement. Fine-needle aspiration of regional lymph nodes, even if they appear normal, is indicated to detect metastases. Melanomas may be amelonotic and can cytologically resemble fibrosarcomas or carcinomas. Biopsy and subsequent histopathologic analysis may be required for a definitive diagnosis.

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Constipation (the infrequent and difficult evacuation of feces) and obstipation (intractable constipation) have several causes. The initial use of symptomatic therapy is often successful, but it is preferable to look for causes, because some problems that are initially treatable may become irreversible if symptomatic therapy masks the signs for too long.

A search of the history for iatrogenic, dietary, environmental, or behavioral causes should be done. Feces should be examined to determine whether they contain plastic, bones, hair, popcorn, or other such material. Physical and rectal examinations are done to search for rectal obstruction or infiltration. Plain pelvic, radiographs can help show whether the animal has anatomic abnormalities or a previously undetected colonic obstruction (e.g., prostatomegaly, enlarged sublumbar lymph node.) Ultrasonography is the preferred technique when looking for infiltrates. Serum biochemistry panel, and urinalysis may reveal causes of colonic inertia.

Colonoscopy is indicated if one suspects an obstruction too orad to be detected by digital examination. Ultrasound-guided fine-needle aspiration of infiltrative colonic lesions sometimes yields diagnostic findings, but colonoscopy (especially rigid) allows a more reliable biopsy specimen to be obtained. If a thorough diagnostic work-up fails to identify a cause in a patient with a grossly dilated colon, then idiopathic megacolon may be present.

Canine and Feline constipation diagnostic plan:

History
Physical examination
Rectal palpation
Abdominal palpation
Abdominal X-rays

Canine and Feline constipation treatment:

Fluid therapy
Laxatives
Enemas
Manual removal of impacted stool
Surgery
Treat primary cause

Canine and Feline constipation dietary plan:

A moderate-to-high fiber diet
Ensure adequate water intake

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Causes of dog and cat diarrhea.

Diarrhea refers to feces containing excessive water. Fecal mucus is principally caused by large bowel disorders. The best approach to the assessment of dogs and cats with diarrhea is to first distinguish acute from chronic problems.

Acute diarrhea is usually caused by diet, parasites, or infectious diseases. Dietary problems are often detected by history; parasites by history and fecal examinations; and infectious diseases by history (evidence of contagion or exposure) and the exclusion of other causes. If acute diarrhea in dogs and cats becomes severe or persistent, additional diagnostic tests are recommended. The approach used is similar to that adopted for the assessment of animals with chronic diarrhea.

Dogs and cats with chronic diarrhea should first be examined for evidence of parasites; multiple fecal examinations looking for nematodes, Giardia, and Tritrichomonas are indicated. Next it should be determined whether the diarrhea is small or large intestinal in origin. Failure to lose weight almost always indicates the presence of large bowl disease; weight loss usually indicates the presence of small bowl disease (pythiosis, histoplasmosis, malignancy). Animals with weight loss resulting from large bowl disease usually have obvious signs of colonic involvement (fecal mucus, marked tenesmus, hematochezia).

Causes of acute diarrhea in dogs and cats:

DIET:
Intolerance/Allergy
Poor-quality food
Rapid dietary change (especially in puppies and kittens)
Bacterial food poisoning

PARASITES:
Helminths
Protozoa
Giardia
Tritrichomonas
Coccidia

INFECTIOUS CAUSES:
Viral causes:
Parvovirus (Feline, Canine)
Coronavirus (Feline, Canine)
Feline leukemia virus

Bacterial causes:
Salmonella
Clostridium perfringens
Verotoxin-producing E. coli
Campylobacter jejuni
Yersinia enterocolitica
Salmon poisoning
Various other bacteria

OTHER CAUSES:
Hemorrhagic gastroenteritis
Intussusception
Irritable bowel syndrome
Ingestion of toxins
Garbage can intoxication (spoiled foods)
Chemicals
Heavy metals
Various drugs (antibiotics, antineoplastics, anthelmintics, anti-inflammatories, digitalis, lactulose)
Acute pancreatitis

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Regurgitation is the expulsion of material (i.e., food, water, saliva) from the mouth, pharynx, or esophagus. It must be differentiated from vomiting (the expulsion of material from the stomach and/or intestines) and expectoration (the expulsion of material from the respiratory tract). Historical and physical examination findings sometimes allow these three to be differentiated. Expectoration is generally associated with coughing at the time of the event. Animals that regurgitate and occasionally those that vomit may cough as a result of aspiration, but oral expulsion is not consistently related with coughing.

Some animals that appear to be regurgitating are vomiting and vice versa. If one cannot distinguish between the two on the basis of the history and physical examination findings, one may use a urine dipstick to determine the pH and whether there is bilirubin in freshly ”vomited” material. If the pH is less that 5, the material has originated from the stomach and probably resulted from vomiting. If the pH is more than 7 and there is no evidence of bilirubin, this is consistent with regurgitation. The presence of bilirubin indicates the material has originated from the duodenum (i.e., vomiting). A positive finding of blood in the urine dipstick test is not useful.

If vomiting and regurgitation still cannot be distinguished, plain and/or contrast-enhanced radiographs will usually detect any existing esophageal dysfunction. However, some esophageal disorders (e.g., hiatal hernia, partial stricture) are easily missed unless a careful radiographic technique is used.

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Unless the dog was seen eating some irritative substance, acute gastritis in dogs and cats is usually a diagnosis of exclusion based on history and physical examination findings. Abdominal radiographs and/or clinical pathologic data are indicated if the animal is severely ill or if other disease is suspected. Once alimentary foreign body, obstruction, parvoviral enteritis, uremia, diabetic ketoacidosis, hypoadrenocorticorticism, hepatic disease, hypercalcemia and pancreatitis are considered unlikely, acute gastritis in dogs and cats is a reasonable tentative diagnosis. If the vomiting resolves after 1 or 2 days of symptomatic and supportive therapy, the tentative diagnosis is considered correct, although pancreatitis must still be considered. Gastroscopy in such animals might reveal bile or gastric erosions/hyperemia.

Because acute gastritis is a diagnosis of exclusion and its signs are suggestive of various other disorders (e.g., foreign bodies, intoxication), good history taking and physical examination are mandatory. The owner should monitor the pet, and if the animal’s condition worsens or if it does not improve within 1 to 3 days, imaging, a complete blood count, a serum biochemistry profile and urinalysis are indicated.

We also recommend this natural balanced real-meat dog food and natural dietary supplement for recovery.
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Dogs are more commonly affected by acute gastritis because of their less discriminating eating habits. Signs usually consist of acute onset of vomiting; food and bile are typically vomited, although small amounts of blood may be present. Affected animals are typically uninterested in food and may or may not feel sick. Fever and abdominal pain are uncommon.

Acute gastritis therapy in dogs principally consists of parental fluid therapy; withholding food and water for 24 hours often suffices to control vomiting. If the vomiting persists or is excessive, or if the animal becomes depressed because of the vomiting, central-acting antiemetics (e.g., prochlorperazine, metoclopramide, ondansetron) may be administered parenterally.

When feeding begins, small amounts of cool water are offered frequently. If the animal drinks without vomiting, small amounts of a bland diet are offered. Antibiotics and corticosteroids are rarely indicated.

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