Panel Co-Chair

All Cats Hospital, P.A.

Largo, Florida

Ilona Rodan, DVM, Diplomate ABVP (Feline Practice)

Panel Co-Chair

Cat Care Clinic

Madison, Wisconsin

Helen Tuzio, DVM, other?

Panel Co-Chair

Forest Hills Cat Hospital

Glendale, New York

Dawn Boothe

Texas A&M Clinical Pharmacology Lab

College Station, Texas

Elyse Kent, DVM, Diplomate ABVP (Feline Practice)

Westside Hospital for Cats

Santa Monica, California

Sara Stephens, DVM, Diplomate ABVP (Feline Practice)

Alpine Veterinary Service

Missoula, Montana

Lauren Trepenier, DVM

University of Wisconsin College of Veterinary Medicine

Madison, Wisconsin

The Guidelines to Judicious Therapeutic Use of Antimicrobials in Cats are designed to provide information to aid practicing veterinarians in choosing appropriate antimicrobial therapy to best serve their patients and to help minimize the development of antimicrobial resistance. Presented below are the Principles of Judicious Therapeutic Use of Antimicrobials as approved by the American Veterinary Medical Association Executive Board, which have been adopted as a framework document for the recommended guidelines developed for cats. This working document will be updated annually by the American Association of Feline Practitioners and the Academy of Feline Medicine Practice Recommendations Committee.

American Veterinary Medical Association Judicious Therapeutic Use of Antimicrobials

(Approved by the AVMA Executive Board - - November, 1998)

When the decision is reached to use antimicrobials for therapy, veterinarians should strive to optimize therapeutic efficacy and minimize resistance to antimicrobials to protect public and animal health.

1. Support development of a scientific knowledge base that provides the basis for judicious therapeutic antimicrobial use.

2. Support educational efforts that promote judicious therapeutic antimicrobial use.

3. Preserve therapeutic efficacy of antimicrobials.

4. Ensure current and future availability of veterinary antimicrobials.

1. Facilitate development and distribution of appropriate antimicrobial use guidelines by practitioner species-interest groups.

2. Improve scientifically based therapeutic practices through education.

1. Improved monitoring and feedback systems for antimicrobial use and resistance patterns.

2. Research to improve scientifically based therapeutic practices.

Preventive strategies, such as appropriate husbandry and hygiene, routine health monitoring, and immunization, should be emphasized.

Other therapeutic options should be considered prior to antimicrobial therapy.

Judicious use of antimicrobials, when under the direction of a veterinarian, should meet all requirements of a valid veterinarian-client-patient relationship.

Prescription, Veterinary Feed Directive, and extralabel use of antimicrobials must meet all the requirements of a valid veterinarian-client-patient relationship.

Extralabel antimicrobial therapy must be prescribed only in accordance with the Animal Medicinal Drug Use Clarification Act amendments to the Food, Drug, and Cosmetic Act and its regulations.

Veterinarians should work with those responsible for the care of animals to use antimicrobials judiciously regardless of the distribution system through which the antimicrobial was obtained.

Regimens for therapeutic antimicrobial use should be optimized using current pharmacological information and principles.

Antimicrobials considered important in treating refractory infections in human or veterinary medicine should be used in animals only after careful review and reasonable justification. Consider using other antimicrobials for initial therapy.1

Use narrow spectrum antimicrobials whenever appropriate.

Utilize culture and susceptibility results to aid in the selection of antimicrobials when clinically relevant.

Therapeutic antimicrobial use should be confined to appropriate clinical indications. Inappropriate uses such as for uncomplicated viral infections should be avoided.

Therapeutic exposure to antimicrobials should be minimized by treating only for as long as needed for the desired clinical response.

Limit therapeutic antimicrobial treatment to ill or at risk animals, treating the fewest animals indicated.

Minimize environmental contamination with antimicrobials whenever possible.

Accurate records of treatment and outcome should be used to evaluate therapeutic regimens.

1In this context, this principle takes into account development of resistance or cross-resistance to important antimicrobials.

Glossary:

Antibiotic--a chemical substance produced by a microorganism which has the capacity, in dilute solutions, to inhibit the growth of or to kill other microorganisms.

Antimicrobial--an agent that kills bacteria or suppresses their multiplication or growth. This includes antibiotics and synthetic agents. This excludes ionophores and arsenicals.

Narrow Spectrum Antimicrobial--an antimicrobial effective against a limited number of bacterial genera often applied to an antimicrobial active against either Gram-positive or Gram-negative bacteria.

Broad Spectrum Antimicrobial--an antimicrobial effective against a large number of bacterial genera; generally describes antibiotics effective against both Gram-positive and Gram-negative bacteria.

Antibiotic Resistance--a property of bacteria that confers the capacity to inactivate or exclude antibiotics or a mechanism that blocks the inhibitory or killing effects of antibiotics.

Extralabel--Extralabel use means actual use or intended use of a drug in an animal in a manner that is not in accordance with the approved labeling. This includes, but is not limited to, use in species not listed in the labeling, use for indications (disease or other conditions) not listed in the labeling, use at dosage

levels, frequencies, or routes of administration other than those stated in the labeling, and deviation from the labeled withdrawal time based on these different uses.

Immunization--the process of rendering a subject immune or of becoming immune, either by conventional vaccination or exposure.

Monitoring--monitoring includes periodic health surveillance of the population or individual animal examination.

Therapeutic--treatment, control, and prevention of bacterial disease.

Veterinarian/Client/Patient Relationship (VCPR) -- A VCPR exists when all of the following conditions have been met:

Veterinary Feed Directive (VFD) Drug--The VFD category of medicated feeds was created by the Animal Drug Availability Act of 1996 to provide an alternative to prescription status for certain therapeutic animal pharmaceuticals for use in feed. Any animal feed bearing or containing a VFD drug shall be fed to

animals only by or upon a lawful VFD issued by a licensed veterinarian in the course of the veterinarian's professional practice.

Although infrequent in kittens and young adult cats, UTIs are a significant and common problem in older cats. The host defenses include normal and complete emptying of the bladder, normal anatomy of the urinary tract, and concentrated urine^{.1, 2} Common diseases of older cats, such as chronic renal failure, diabetes mellitus, and hyperthyroidism, affect the urine osmolality causing dilute urine and predispose the cat to UTIs. ^{2, 3} In recent studies, approximately 20-30% of cats with chronic renal failure, primarily females, had bacterial UTIs ^{3,4, 5}. Other conditions that impair host factors and predispose to infection include urinary obstruction; catheterization, especially indwelling catheterization, and perineal urethrostomy.

Since many cats with UTIs present with nonspecific signs or are asymptomatic, urinalyses should be included in preventive health screening tests to help detect early or silent UTIs. Upper urinary tract infections UTIs are usually caused by organisms that normally inhabit the intestinal or lower urogenital tracts ascending the urethra. E. coli is the most common cause of infection

Diagnostics: Urinalysis, including sediment evaluation, is important to identify or exclude other underlying abnormalities and can suggest UTI. In cases of decreased specific gravity and where there is little or no inflammatory response, urine culture is necessary to make a diagnosis. Since decreased specific gravity predisposes to UTI, urine culture is indicated in cats with low specific gravity regardless of findings on urinalysis.

Urine should be collected by cystocentesis before initiating antimicrobial therapy and the administration of fluids. Bacteria present in samples collected by cystocentesis are indicative of infection, unless skin contamination or accidental bowel penetration occurs. Midstream collection of urine may be necessary in severely dysuric cats. If the sample is collected mid-stream, it should be done as cleanly as possible and into a sterile container

A complete urinalysis, including sediment evaluation, should be performed. Dipstick leukocyte assays and dipstick assays for bacteria are inaccurate and should not be used. Microscopic evidence of bacteriuria and pyuria are suggestive of bacterial UTI. However, pyuria can indicate either inflammation or infection, and it is essential to differentiate between these by urine culture to avoid unnecessary antimicrobial therapy. Brownian movement, amorphous debris and contamination may all lead to a false diagnosis of UTI from urine analysis alone.

Qualitative urine culture includes organism identification and sensitivity. Because inadvertent contamination can occur, quantitative urine culture, which measures the number of bacteria in addition to identifying the organism, is the preferred method. This is especially important for samples that cannot be collected by cystocentesis. A small volume of urine must be submitted for quantitative urine culture. Urine should be cultured immediately or may be refrigerated for up to 6 hours. If the veterinary practice cannot deliver samples to the lab in a timely fashion, urine should be cultured onto blood agar plates. Most UTIs involve a single bacterial species, with >100,000/ml.

Susceptibility testing helps identify appropriate antibiotics to treat the infection. The ADD test (Kirby-Bauer) determines bacterial sensitivity or resistance based on plasma or serum drug concentrations, and not urine concentrations. Most antimicrobials are renally excreted and therefore present in much higher concentrations in urine than in blood as long as the as the drug is excreted in the active form by the kidney and renal function is normal. To prevent the inaccuracies that result from differences in urine versus plasma concentrations of antimicrobials, the MIC for a panel of antimicrobials for each infective agent should be established.¹ This means that if a susceptibility test determines that an isolate is only moderately susceptible to a specific antibiotic, that antibiotic may still be effective for a lower urinary tract infection because the drug concentration in the urine may be much higher than that of the plasma or serum.

Due to the difficulty in localizing UTIs, one must often rely on a combination of clinical signs (Table 2), diagnostic tests, and response to therapy.⁷ Clinical signs consistent with renal involvement are suggestive of pyelonephritis. Neutrophilic leukocytosis with a left shift may be present in cases of acute pyelonephritis. The white blood cell count is normal in most cases of bacterial cystitis, urethritis, and chronic pyelonephritis. Non-regenerative anemia may be present with chronic pyelonephritis due to anemia of chronic disease and/or secondary to chronic renal failure. Azotemia often exists in chronic pyelonephritis. Radiographs and/or ultrasound can also help to localize the infection and identify the underlying cause of UTI, such as abnormal kidney size or radiopaque uroliths. Fine needle aspirate from the kidney or renal pelvis and positive bacterial culture can also be done to localize and confirm pyelonephritis.

Non-Antimicrobial Interventions: In addition to antimicrobial therapy, every attempt should be made to identify and correct the underlying abnormalities in host defenses that predispose to UTIs. Fluid therapy to correct dehydration and/or promote diuresis should also be given as needed.⁴

Antimicrobial Treatment Intervention: Although antimicrobial therapy should be based on urine culture and sensitivity results, it is often in the best interest of the patient to begin therapy pending sensitivity results. In suspected pyelonephritis, or while awaiting sensitivity results, inference is based on urine pH and whether there are rods or cocci present in the urinalysis. (Table 1)

Acidic Rods E. coli Enrofloxacin

Acidic Cocci Enterococcus- Amoxicillin

Streptococcus

Alkaline Rods Proteus mirabilis Amoxicillin

Alkaline Cocci Staphylococcus Cephalexin

Nephrotoxic antimicrobials (aminoglycosides and tetracyclines, excluding doxycycline) should be avoided, especially in cases of known or potential cases of renal compromise. Drug doses should be altered for drugs excreted by the kidneys if there are decreases in creatinine clearance or elevations in serum creatinine.

Treatment Duration: Therapy should be sufficient to eradicate urinary pathogens, and duration depends upon location of infection, chronicity and recurrence, and whether it is possible to correct underlying abnormalities. The only way to ensure that the antimicrobial is effective is by reculturing the urine during (a few days after starting therapy) and after treatment (1 week after concluding therapy).²

Treatment for acute bacterial cystitis usually requires 7-14 days of antimicrobial therapy when repeated urine cultures are negative. For chronic infections (regardless of location) or pyelonephritis, treatment should be continued for a minimum of 4-6 weeks. For relapsing or persistent UTIs, antimicrobial therapy is indicated for a minimum of 6 weeks. Urine culture should be repeated for all of the above on a periodic basis following therapy: 1 week and 1, 2, 3, 6, 9, 12, 18, and 24 months.² If bacteriuria recurs with discontinuation of therapy for relapsing or persistent infections, the patient should be treated for 4-6 months.

Suppressive or prophylactic therapy is indicated if relapses occur every time antimicrobial therapy is stopped. Causes of treatment failure include inappropriate drug, dose, inappropriate duration of therapy, lack of client compliance, failure of the drug to reach sufficient concentrations in urine (e.g., due to lack of intestinal absorption of the drug, impaired renal function, or development of antimicrobial resistance), a nidus of infection (e.g., pyelonephritis, urolith, persistent patent urachus, neoplasia) exists, and decreased resistance to bacterial colonization due to abnormal urination or anatomic defect.

Suppressive therapy can be instituted once the urine is sterile following full dose therapy. A single dose (1/2 to 1/3 of the usual daily dose) per day is given, preferably at night or when urine will be held for several hours to allow for high concentration of antibiotic in urine. Risks include antimicrobial toxicity and bacterial resistance. Urine should be collected by cystocentesis and cultured every 4-6 weeks to ensure that the drug remains effective.² If urine remains sterile for 6 months, antimicrobial therapy can be discontinued, and urine should be re-cultured at 1 week and 1, 2, 3, 6, 9, 12, 18, and 24 months. If infection recurs, it should be treated with full-dose therapy followed by reinstituting prophylactic therapy.

Treatment Assessment: Urine culture should always be repeated several days after the end of treatment to ensure that the medication was successful in resolving the infection. In addition, at least when treating empirically, urine culture should be repeated during treatment. 1

Client education and followup are essential for treatment success. Clients must understand the importance of completing antimicrobial therapy or contacting the veterinarian if adverse reaction prevents completion of the antibiotic dose. They should understand that ameliorization of clinical signs does not necessarily indicate resolution of UTI, and that recurrent or continued infections can occur. Followup with recheck urine culture is the only reliable assessment of treatment.

Prevention should be directed at correcting underlying problems. Whenever it is impossible to correct underlying host defenses, regular patient follow-ups, including urine culture, aid in early diagnosis and treatment. Long-term, low dose antimicrobial therapy should only be used in relapsing infections to prevent frequent use of high doses of antimicrobials.

Introduction: Vast numbers of bacteria are found everywhere on the epithelial surfaces of the oral cavity and oropharynx and in the gingival sulcus. The predominant oral microorganisms are anaerobes, which play an important role in protecting the mucosal surfaces from interactions with potentially pathogenic aerobes by producing metabolic by-products that limit the number of aerobes able to coexist with them. The normal flora of the oral cavity are often comprised of the same microorganisms isolated from obvious infections in the region.

Where oxygen supply can easily reach an infected area of gingiva or oral tissue, aerobes such as Staphylococcus spp. and Streptococcus spp. are commonly isolated. Coliforms, Pseudomonas and Pasteurella are frequently present as well. Diseased areas that are deep in tissue or beneath teeth where they are somewhat protected from extrinsic oxygen supply tend to support anaerobic microorganisms. A wide range of anaerobic bacteria such as Bacteroides, Fusobacterium, Peptostreptococcus, Porphyromonas, Prevotella, Campylobacter and spirochetes will predominate within an abscess or necrotic neoplastic tissue or where oxygen is depleted by bacterial metabolism.

Documented or presumed bacterial processes in the oral cavity include periodontal disease, gingivitis, stomatitis, faucitis, endodontic apical abscessation, foreign body penetration and abscessation, necrotic, infected eosinophilic granuloma complex lesions, and ulcerated oral neoplasia with secondary bacterial invasion.

Diagnostics: For the purpose of culture, tissue samples often yield a more representative population of pathogenic bacteria than do samples collected by sterile swab. Samples from an abscess should include pus and a portion of the wall of the abscess. Tissue specimens should be placed (unfixed and without preservatives) in sealed sterile containers to prevent contamination or desiccation.

If anaerobic as well as aerobic bacteria cultures are collected from any of the aforementioned infections, one can expect to isolate an average of 4-6 organisms. An average of 2 of these will be anaerobes, almost always accompanied by one or more aerobes. In general, greater than 80% of oral and gingival pathogens will likely be obligate anaerobes.

As a general rule, isolation of a mixture of 4 or more aerobic microorganisms in light or moderate numbers is characteristic of normal oral flora. The problem then arises of deciding which, if any, of multiple isolated organisms are "significant" in the disease process. In addition, not all clinical laboratories are experienced in processing oral samples, therefore many important organisms can be missed due to inadequate anaerobic culture techniques.

There are few situations in which culture is recommended. These include deep seated prolonged infection of maxillary or mandibular bone, persistence of one or more fistulous tracts, and lack of response to antibiotics most likely to be effective.

Antimicrobial Treatment Intervention: Bacterial isolates in gingivitis and susceptibility of selected anaerobes to antimicrobial agents are summarized in Table 2.

Table 2. Treatment Regimens for Oral Cavity Infections

Superficial ulcers (mixture of aerobes and anerobes Amoxicillin-clavulanate (Clavamox®,

or combination of superficial/deep infections Pfizer Animal Health)

Ulcerative stomatitis (oral anaerobes) Metronidazole

Deep periodontal pockets (mainly anaerobic Amoxicillin-clavulanate (Clavamox®,

Long-standing infection that has reached beyond the Clindamycin (Antirobe®, Upjohn)

periodontal pocket into bone (anaerobic bacteria)

Gram-negative aerobic infection Enrofloxacin (Baytril®, Bayer)

A few select concurrent systemic circumstances are indications for antimicrobial use when they accompany oral disease. These include cats with clinical evidence of cardiac disease, advanced hepatic or renal disease or immunocompromised patients.

A special emphasis needs to be made regarding the use of antimicrobials for periodontal disease as this is the single most common disease in cats. It is documented and agreed upon that complete prevention of accumulation of bacterial plaque absolutely inhibits development of gingivitis and receding gingiva. There is controversy over whether the long term use of antimicrobials is beneficial in treating periodontal disease. Short-term use of antimicrobials around and shortly after dental cleaning and extractions or restorations has been shown to be beneficial.

Introduction: Feline abscess formation is frequently the result of a previous bite wound from another cat. Unlike a bite wound from a dog, which is generally a laceration and tearing of the flesh, a bite from another cat usually results in a deep puncture wound. The surface of the injury usually heals quickly, but the bacteria deposited from the bite are left to multiply deep in the tissues. Clinical infection usually is not evident for two to four days post-trauma. Bite wounds occurring where the skin and underlying tissues are tightly adherent generally result in a cellulitis. Abscesses, on the other hand, usually appear as painful, well-demarcated fluctuant masses most commonly on the face, neck, tail or trunk, where the skin is loose

Diagnostics: A presumptive diagnosis may be based on history and clinical signs. A hemogram generally reveals a leukocytosis and neutrophilia. The exudate should be cultured for both aerobes and nonaerobic bacteria.

Non Antimicrobial Interventions Initial therapy relies on surgical drainage and debridement of the abscessed area. Small areas may be drained ventrally, explored and flushed well; some may require drain placement. Very large cavities may be packed open for several days with medicated gauze, followed by the application of warm compresses and topical agents that will protect the granulating tissue.

Antibiotic Treatment Intervention: Broad-spectrum systemic antibiotics are indicated both in cases of cellulitis and abscess formation. The choice of antibiotic should ideally be based on culture and sensitivity results. The organisms identified in abscesses are generally normal oral flora. The most common pathogen is P. multocida, but beta-hemolytic streptococci, Fusobacterium spp., and spirochetes are commonly implicated. Less commonly seen are E. coli, Bacteroides, Actinomyces, Clostridium, Peptostreptococcus, and Propionibacterium. In many cases, more than one bacterium is identified. While awaiting culture and sensitivity results the antibiotics of choice are the penicillins. Amoxicillin and clavulinic acid (Augmentin, Clavamox) has a spectrum of activity that includes most organisms found in animal bite wounds. Systemic therapy should be continued for five to ten days, depending on manufacturer’s instructions and the veterinarian’s clinical judgment.

Other Treatment Considerations: Since feline leukemia virus and feline immunodeficiency virus are transmitted by bite wounds, these diseases must be discussed with the owner, and future testing for the presence of these viruses should be recommended. In recurrent cases or non-healing wounds, immediate testing may be warranted, as well as tissue biopsy to rule out underlying lymphosarcoma or squamous cell carcinoma. Mycoplasma and fungal organisms should also be considered in unresponsive cases.

Prevention: Since bite wounds and abscesses are most common in intact males, castration is recommended to reduce the incidence of cat fights. In addition, if given within 24 hours of a catfight, a single injection of penicillin G has been shown to be effective against abscess formation.

Cholangitis is an inflammatory process limited to the bile ducts within the liver parenchyma with no hepatic involvement. Cholangiohepatitis is an inflammation of the intrahepatic bile ducts and adjacent hepatocytes.

Cholangitis/Cholangiohepatitis Complex has three histopathologic lesions: suppurative cholangitis/cholangiohepatitis, nonsuppurative cholangitis/cholangiohepatitis, and biliary cirrhosis.

Some cats with suppurative cholangitis or cholangiohepatits may be asymptomatic or present with vague signs such as lethargy or inappetance. However, most cats with cholangiohepatitis present with clinical signs referable to hepatic disease. These symptoms include vomiting, anorexia, weight loss, depression, fever, and icterus. The onset of disease may be an acute or insidious. Physical examination findings often reveal icterus, dehydration and weight loss, except when biliary cirrhosis is present, when ascites may be present.

Diagnostics: In some cats with mild suppurative cholangitis, a leukocytosis may be the only hematologic abnormality. With hepatic involvement, there are frequently elevations in bilirubin, alkaline phosphatase (SAP), and alanine aminotransferase (ALT) on a biochemical profile, and bilirubin and urobilinogen may be found in the urine. A presumptive diagnosis may be made on fine needle aspirate of the liver, but a liver biopsy is required for a definitive diagnosis. Liver tissue should be cultured for aerobes and anaerobes.

Non Antimicrobial Intervention: Nonsuppurative (lymphocytic) cholangitis/cholangiohepatitis is an inflammatory condition, so corticosteroids are the cornerstone of therapy. Prednisolone is generally used at immunosuppressive doses until remission is achieved. Antibiotics are not likely to be helpful unless bacteria are isolated. However, they are generally recommended in this condition along with intense cortisone therapy. These cats require supportive and symptomatic treatment. Dehydration must be corrected with an intravenous infusion of an isotonic fluid. In addition, vomiting should be controlled with the use of anti-emetics such as metoclopramide. Agents such as dehydrocholic acid have been recommended to improve bile flow. Cats with biliary cirrhosis are in irreversible hepatic failure and generally die despite supportive care.

Antimicrobial Treatment Intervention: Antibiotics are definitely indicated in the suppurative form of the disease, since bacteria are generally the causative agent. The choice of antibiotic should be made based on the results of aerobic and anaerobic cultures of liver tissue. However, when these are not available, the antibiotics chosen should be ones that are not hepatotoxic while reaching high concentrations in bile, and are effective against anaerobes and coliforms, since the most common organisms isolated from affected tissues are E. Coli and gram positive anaerobes. Enterococcus, Bacteroides, Fusobacterium and a-hemolytic strep have also been reported in acute cases. Amoxicillin and ampicillin are the most widely recommended antibiotics, although enrofloxacin is thought to be useful as well, and cephalexin also has been used. Since enrofloxacin is ineffective against anaerobes, it is generally combined with one of the penicillins. Metronidazole is another excellent choice, since it is effective against anaerobes and penicillin-resistant bacteria; it may be combined with amoxicillin or ampicillin.

Other Treatment Considerations: The prognosis for the suppurative form of the disease is highly variable, ranging from complete recovery to severe exacerbation and eventual biliary cirrhosis. Those with the chronic form are also subject to relapse following withdrawal of therapy. In either case, the patient must be monitored closely on a long-term basis. Sequelae that may occur as a result of either form are bile sludging and/or cholelithiasis which can lead to biliary obstruction. In some cases, inspissated bile and/or choleliths may need to be removed surgically. An obstruction of the biliary system may progress to a "white bile syndrome" in which the gallbladder secretes fluid and mucus in the absence of bile. The prognosis in these cases is poor. Hepatic encephalopathy occurs very rarely and should be treated accordingly.

Prevention Strategies: The etiology and pathogenesis of feline cholangiohepatitis is poorly understood. Although the underlying etiology is thought to be an ascending infection by enteric bacteria, the initiating mechanism is not fully understood, so preventive measures are difficult to outline. Certainly, early diagnosis aids in the successful treatment, since persistent hepatic inflammation often leads to progressive fibrosis and eventual cirrhosis.

2. Uncomplicated Upper Respiratory Infection

Systemic antibiotics are frequently administered therapeutically when a kitten or adult cat is presented with acute clinical signs of viral rhinitis or rhinotracheitis. Clinical signs include clear watery nasal discharge, epiphora and mild signs of conjunctivitis, and sneezing. These cats may or may not be febrile and usually have no history of anorexia. When the aforementioned signs are non-progressive and subside in 7 to 10 days, oral or parenteral antibiotics are not indicated.

Primary bacterial rhinitis is extremely rare in the cat. The signs of bacterial rhinitis or rhinotracheitis include sneezing, mucopurulant nasal discharge, possible mucopurulant ocular discharge, and coughing with retching or gagging. Cytologic specimens of exudates in bacterial rhinitis or rhinotracheitis cases will be consistent with septic, purulent exudates. Bacterial cultures are confusing and difficult to interpret because they often yield a mixed population similar to that of normal nasal flora. Very occasionally, a pure culture of a pathogen will help you choose an appropriate antibiotic through susceptibility testing. It is only justifiable to perform cytological and culture and susceptibility testing in a sneezing cat when signs of bacterial rhinitis predominate or if traditional viral respiratory signs last longer than two weeks.

Fever is a common presenting sign in the cat and is associated with many infectious and non-infectious conditions. The indiscriminate use of antibiotics should be avoided as they may interfere with clinical signs and the results of subsequent laboratory tests. A complete history including information about environment, travel, reproductive status, and previous medical problems and surgical procedures along with a comprehensive medical examination will help direct the diagnostic plan. An initial laboratory database should include a complete blood cell count including examination of a blood smear for parasites and intracellular pathogens, a serum biochemistry profile, feline leukemia virus antigen test, feline immunodeficiency virus antibody test, complete urinalysis including microscopic sediment examination (bacterial culture and sensitivity if inflammatory cells are noted in the sediment) and non-contrast radiographs of the thorax and abdomen. Other diagnostic tests such as contrast radiographic studies, dental radiographs, serologic studies, blood culture, ultrasonography, bone marrow aspiration and biopsy, percutaneous fine-needle aspiration, transtracheal washes, bronchoalveolar lavage, and endoscopy may be necessary to determine the cause of the fever. Exploratory laparotomy should be a procedure of last resort. Treatment should always be directed toward the underlying cause of the fever whenever possible. However, when a patient's condition is deteriorating, a therapeutic trial with a broad-spectrum combination of antibiotics may be a the least harmful and most helpful treatment. Recommended antibiotic combinations penicillin and an aminoglycoside or a cephalosporin and an aminoglycoside .

I attempted to shorten this section, but found it impossible to condense the information into a paragraph or two. Perhaps Dawn could do this.

The role of resistance in therapeutic failure of antimicrobials is well established (Neu, 1994; Tomasz, 1994). The ability of organisms to develop resistance to antimicrobials varies with the species and strain. Resistance may be inherent or acquired. Inherent resistance is exemplified by the lack of efficacy of aminoglycosides against anaerobic organisms since the drugs must be actively transported into the cell (oxygen dependent). Acquired resistance can occur during the course of therapy (leading to changes in a culture and susceptibility pattern). Acquired resistance can reflect a mutational change, ie, a chance mutation in the genetic material, or the transfer of genetic material between organisms, usually in a plasmid. Mutational resistance occurs slowly, and often is accompanied by other changes that render the organism less viable and thus more likely to be destroyed by other drugs, etc. Transduction (especially by Staphylococcal organisms; material is copied by a phage) and transformation are less common methods by which organisms can acquire extrachromosomal DNA. In contrast to mutational resistance, plasmid mediated resistance, particularly that transmitted by conjugation, is a clinically relevant method of transfer that impacts therapeutic success. Plasmid-mediated resistance in gram-negative organisms is common, can develop rapidly and can be transmitted between species. A single transfer of plasmid genetic material from a bacterial donor can result in antimicrobial resistance against up to seven antimicrobials in the recipient bacterial cell during therapy.

The mechanisms of bacterial resistance vary and involve changes in cell wall structures, proteins (ie, penicillin-binding proteins), or enzymes; development of enzymes which destroy antimicrobials (ie, ß-lactamases which destroy penicillins, Figure 3), and changes in intracellular transport proteins (tetracyclines), metabolic pathways (sulfonamides) or binding sites (ie, on ribosomes as for aminoglycosides) for antibiotics. Bacteria will often respond to the presence of the antimicrobial by altering their physiology such that resistance occurs. Organisms are likely to have more than one mechanism of resistance. One of the reasons that Pseudomonas sp. is so difficult to treat is its ability to alter porin size in response to the presence of an antimicrobial. Smaller porin sizes preclude drug movement through the lipopolysaccharide capsule. Beta-lactamase formation is inducible in Staphylococcus sp.; formation greatly increases in the presence of a b-lactam antibiotic.

The recent recognition of impaired efficacy of antimicrobials that have traditionally been very effective for treatment of infections has underscored the significance of antimicrobial resistance. Plasmid-mediated resistance is of particular concern because of its rapid onset and the potential for transmission among species of microbes.

Actions should be taken to avoid antimicrobial resistance, not only for the patient, but also for the medical community. Even if an antimicrobial is characterized by a low incidence of plasmid-mediated resistance (such as enrofloxacin), resistance to drugs takes several decades to develop. Thus, actions should be taken proactively such that the likelihood of resistance developing against a group of antimicrobials is reduced.

The recent use of antimicrobials in the patient should be considered when selecting an antimicrobial (Neu, 1994). The development of infection despite recent or ongoing antimicrobial therapy suggests that the infecting organism is resistant to the antibiotic chosen. Basing drug selection on culture and susceptibility information is probably the best method to reduce the risk of resistance. However, secondary resistance can also occur during the course of antimicrobial therapy, even if selection is based on culture and susceptibility data. Pharmaceutical manufacturers have been able to manipulate antimicrobial drugs in a variety of ways such that resistance is minimized and these options can be selected in an attempt to minimize resistance. For example, bacterial resistance has been decreased by: synthesizing smaller molecules that can penetrate smaller porins (eg., the extended spectrum penicillins, ticarcillin and piperacillin); "protecting" the antibiotic (eg, clavulanic acid which "draws" the attention of the b-lactamase away from the penicillin); modifying the compound so that it is more difficult to destroy (eg, amikacin which is a larger, and more difficult to reach molecule compared to gentamicin); and the development of lipid soluble compounds that are more able to achieve effective concentrations at the site of infection (eg, doxycycline compared to other tetracyclines).

Probably the single most important action that can be taken to reduce the incidence of resistance is to assure that adequate drug concentrations are reached at the site of infection. The development of resistance in critical or chronic situations can be minimized by assuring organisms are exposed to maximum drug concentrations for a sufficient period of time. Thus IV administration should be considered in selected situations such as life threatening conditions or prophylactic therapy, or for difficult to penetrate tissues; doses should be maximized and based on MIC or therapeutic drug monitoring whenever possible; and the proper dosing interval should be used. Host factors should be considered in the design of the dosing regimen. Drugs inherently more resistant to bacterial inactivation should be selected (ie, amikacin rather than gentamicin). Combination antimicrobial therapy (such as b-lactamase protected antimicrobial combinations

1. Senior, David F., The Use of Enrofloxacin in the Management of Urinary Tract Infections in Dogs and Cats, Suppl. Compendium of Continuing Education Pract Vet, Vol 18(2), 1996, pp. 89-95.

2 Polzin, David J, Managing difficult bacterial urinary tract infections, Waltham Focus Vol 7, No 1. 1997, pp. 13-19.

3. Demetriou, Barber & Elliott, Influence of Urine Concentration on Growth of Bacteria in Feline Urine, WSAVA, BSAVA & FECAVA World Congress Congress Synopses ad Clinical Research Abstracts; C. Lamb (ed), April 3-6, 1997, International Convention Center, Birmingham, UK. p. 241.

4. Kerl, Marie E., Feline Bacterial Urinary Tract Infections: Clinical Presentation and Diagnosis, ACVIM 17th Proceedings, Chicago, IL 1999, pp. 28-29.

5. Barber, et al., Incidence and prevalence of bacterial urinary tract infections in cats with chronic renal failure, ACVIM 17th Proceedings, Chicago, IL 1999, p. 716.

6. Osborne, Carl A., Three Steps to Effective Management of Bacterial Urinary Tract Infections: Diagnosis, Diagnosis, and Diagnosis, The Compendium for Continuing Education, Vol. 17, No. 10, October 1995, pp. 1233-1248.

7. Rubin, Stanley I, The procedures that confirm and localize a urinary tract infection, Veterinary Medicine, 1990, pp. 352-364.

8. Papich, Mark G., Antimicrobial Drugs for Pediatric and Geriatric Patients, Pfizer, Feb. 21, 1996, pp. 61-67.

9. Lane, India F., Pharmacologic Management of Feline Lower Urinary Tract Disorders, Veterinary Clinics of North America: Small Animal Practice, Vol. 26, No. 3, pp. 515-533.

1. Aucoin, D, (Consult Sara for details)
2. Hardie, E.M.: Perisurgical Use of Antibiotics, In Managing Microbes, Pfizer, 2-21-96.
3. Harvey, C.E.: Plasmocytic-lymphocytic stomatitis, In August JR (ed): Consultations in Feline Internal Medicine, ed 2, Philadelphia, WB Saunders, 59, 1994.
4. Harvey, C.E., Shafer, F.: Epidemiology of periodontal and oral conditions in cats, J Vet Dentistry, 1996.
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8. Jones, R.L.: Laboratory Diagnosis of Bacterial Infections, In Greene, CE (ed), Clinical Microbiology and Infectious Diseases of the Dog and Cat, 2^nd Edition, Philadelphia, WB Saunders, 179, 1990.

Bibliography – Bite Wounds & Abscesses

Davidson, Ellen B. Managing Bite Wounds in Dogs and Cats. Parts I & II. The Compendium of Continuing Education. vol 20 no 7 July 1998, vol 20 no 9 September 1998.

Hall, Iain A. and Campbell, Karen L. Antibiotic-Responsive Dermatoses. In: Consultations in Feline Internal Medicine. John R. August, ed. 2^nd ed. W. B. Saunders Company. 1994

Macgregor, Rob Roy. Infections caused by animal bites and scratches. In: Harrison’s Principles of Internal Medicine, 12th edition, McGraw-Hill, Inc. 1991

Norsworthy, Gary D. Selected Surgical Procedures. In: Feline Practice. J. B. Lippincott Company. 1993.

Pavletic, Michael M. Wound management in small animal practice. In: Veterinary Emergency and Critical Care Medicine; R. Murtaugh and P. Kaplan, eds. Mosby Year Book. 1992

White, Stephen D. Review Article: Systemic treatment of bacterial skin infections of dogs and cats. Veterinary Dermatology vol 7 1996

Bibliography – Cholangitis/Cholangiohepatitis

Day, Deborah. Feline Cholangiohepatitis Complex. Veterinary Clinics of

North America: Small Animal Practice. Vol 25 No. 2, March 1995.

Ferguson, Duncan C. Rational Empirical Antimicrobial Therapy in Smal

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Jackson, Mark W., Panciera, David L., and Hartmann, Faye. Administration

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a cat. JAVMA 204:4, February 15, 1994 p 602 - 605.

Norsworthy, Gary D. Cholangitis/Cholangiohepatitis Syndrome. In:

Feline Practice. J. B. Lippincott Company. 1993.

References – inappropriate use of antimicrobials in LUTD

1. Kruger, Osborne, et al., Feline Lower Urinary Tract Disease, The Michigan State Experience, Proc. 15th ACVIM Forum, Lake Buena Vista, FL, 1997, pp. 340-342.

2. Kruger, Osborne, Lulich, Management of Nonobstructive Idiopathic Feline Lower Urinary Tract Disease, Veterinary Clinics of North America:Small Animal Practice, Vol 26, No 3, May 1996, pp. 571-588.

3. Kalkstein, Kruger and Osborne, Feline Idiopathic Lower Urinary Tract Disease. Part IV. Therapeutic Options, Compendium, Vol. 21, No. 6, June 1999, pp. 497-509.

4. Lane, India, Pharmacologic Management of Feline Lower Urinary Tract Disorders, in Veterinary Clinics of North America: Small Animal Practice, Vol 26, Number 3, May 1996, pp. 515-533.

5. Lane, India and Bartges, Joseph, Treating refractory idiopathic lower urinary tract disease in cats, Veterinary Medicine, July 1999, pp. 633-641.

6. Osborne, et al., Prednisolone Therapy of Idiopathic Lower Urinary Tract Disease A Double-Blind Clinical Study, Veterinary Clinics of North America:Small Animal Practice, Vol 26, No 3, May 1996, pp. 663-569.

7. Barsanti, et al., Effect of Therapy on Susceptibility to Urinary Tract Infections in Male Cats with Indwelling Urethral Catheters, Journal of Veterinary Internal Medicine, 6:64-70, 1992.

8. Marks, Straeter-Knowlen, Moore, Effects of Acepromazine Maleate and Phenoxybenzamine on urethral pressure profiles of anesthetized, healthy, sexually intact male cats, American Journal of Veterinary Research, 57: 1497-1500, 1996.

9. Buffington, Tony A., Chew, Dennis, Diet therapy in cats with lower urinary tract disorders, Veterinary Medicine, July 1999, pp. 626-630.

10. Polzin, David J., Managing difficult bacterial urinary tract infections, Waltham Focus. Vol 7, No 1, 1997, pp. 13-19.

11. Johnson, Justine & Murtaugh, Robert, Preventing and Treating Nosocomial Infections. Part I. Urinary Tract Infections and Pneumonia, Compendium of Continuing Education, Vol. 19, No. 5, May 1997, pp. 581-586.

12. Civetta, Civetta & Ball, Decreasing catheter-related infection and hospital costs by continuous quality improvement, Critical Care Medicine, Vol. 24, No. 10, 1996, PP. 1660-1665.

1. Foid, R.B.: How to Treat Respiratory Tract Infections, "Managing Microbes", 13, 2-21-96.
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