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Microbial Diseases S to Z
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Table of Content
Salmonellosis
Sarcoid
Sporotrichosis
Strangles
Tetanus
Tuberculosis
Tularemia
Tyzzer's Disease
Urinary Tract Infections
Vesicular Stomatitis
West Nile Virus Infection*
Zygomycosis (Basidiobolomycosis, Conidiobolomycosis)
Salmonellosis
Salmonellosis is a contagious, enteric, bacterial disease of many animals and humans characterized by infections ranging from subclinical to septicemic.
Cause
Salmonellosis is caused by over 2000 serotypes of the gram-negative rod of the genus Salmonella. There are several classification systems for members of the genus. We will use the traditional species names of which each represents a particular serotype. New serotypes are given species names based on where they were isolated.
Some Salmonella species show a host predilection. The following species have been implicated frequently in equine salmonellosis:
- Salmonella typhimurium (probably the most common and most pathogenic)
- S. enteritidis
- S. agona
- S. newport
- S. heidelberg
- S. anatum
Other species have been and will be involved. It is important to remember that there are no host-adapted Salmonella spp., in horses.
All salmonellae are facultative intracellular parasites. There are frequently a number of subclinical carriers in a stable that shed salmonellae intermittently. These carriers constitute the reservoir of the disease and the carrier rate varies considerably from one stable to another.
Transmission
Infection is acquired by ingestion of mainly food and water contaminated with feces from infected or carrier equids.
Occurrence
The disease is worldwide in distribution and some horses in stables, farms and clinics are carriers. In horses, various stresses, e.g., long distance transport, deworming, strenuous training, surgery, overcrowding, and parturition, can trigger serious individual cases and outbreaks. Foals are particularly prone to the septicemic form. Acute and chronic enterocolitis are seen most commonly in older animals.
Salmonellosis is frequently a problem in transported horses and in hospitalized animals in equine clinics.
Pathogenesis
This is very complex and the following is a considerable simplification. First there is attachment of salmonellae primarily to M cells within the epithelium. This is followed by penetration through and between mucosal cells into the lamina propria. Release of endotoxin and enterotoxin contributes to fever, leukopenia, inflammation, hemorrhage, necrosis, shock, and disseminated intravascular coagulation and diarrhea. The infection may be limited to the intestine and adjacent mesenteric lymph nodes by phagocytic cells. Salmonellae have the capacity to survive within macrophages and thus sustain the infection. Varying degrees of necrotic colitis is produced. Bacteremia occurs infrequently in this enterocolitis stage of the disease.
Various stresses contribute to bacteremia which may give rise to sepsis. If the latter is not fatal there is dissemination to various organs including lungs, joints and the gravid uterus. Pneumonia, abortion, meningitis, polyarthritis, osteomyelitis are some of the sequellae. In adults, laminitis is a major potential complication that may occur in association with salmonellosis.
Clinical Features
Release of prostaglandins by enterotoxins activates adenylyl cyclase resulting in enhanced intestinal fluid and electrolyte secretion. Endotoxin producing septic shock is thought responsible for the severity of the disease and death sometimes in less than 24 hours.
Clinical signs depend on the severity of the infection from mild, to acute enterocolitis and most severe, septicemia.
Acute salmonellosis is characterized by fever, depression, anorexia, severe enteritis, watery diarrhea, and rapid dehydration. Signs are similar but less severe in the less acute disease. Survivors are sometimes carriers and thus shedders. In carriers the organism may persist in the mucosa of the colon and cecum and in mesenteric lymph nodes.
Neonatal foals are subject to septicemic salmonellosis and those that survive, may infrequently have neurological complications and/or polyarthritis.
Diagnosis
Salmonellosis is such a serious disease of horses that if suspected a laboratory diagnosis should be sought. All of the diseases, in which chronic and acute gastroenteritis are seen, should be considered. Potomac horse fever, clostridial enterotoxemia, and several idiopathic enteric diseases should be taken into account.
- Feces taken from the rectum are satisfactory for culture. Feces collected on a swab are sufficient in an animal showing clinical signs; however, to detect carriers, 10 - 50 g of feces should be cultured. Five negative fecal cultures on successive days will usually indicate the animal is not infected.
The culture of rectal biopsies rather than feces is sometimes performed to increase test sensitivity. A PCR procedure has been developed for the examination of feces. - From necropsied animals (sick or dead) portions of intestine, liver, spleen, lung, tonsil, and mesenteric lymph nodes are cultured.
- Formalized portions of the above-mentioned tissues are appropriate for histopathology.
- It is not usually difficult to recover salmonellae from animals that have died as a result of salmonellosis. Salmonellae recovered from lymph nodes and vital organs are especially significant. The finding of the characteristic lesions of salmonellosis is supportive.
- Carrier animals shed salmonellae intermittently and, as mentioned above, three to five negative cultures on successive days will usually indicate there is no intestinal infection.
Treatment
- Antimicrobial drugs may be used after susceptibility tests are conducted, although their value is questionable. Strains that are resistant to more than one drug are common. It may not be possible to eliminate the carrier state.
- If used, antibiotics are administered to adult horses during the acute stage of disease when the leukopenia is severe. In young foals, antibiotics are administered through the course of disease to prevent dissemination to multiple organs.
- Fluid and electrolyte replacement. Non-steroidal anti-inflammatory drugs (NSAID) such as flunixin meglumine are used to cope with pain and the systemic effects of endotoxemia.
Prevention
- Efforts should be directed toward minimizing exposure, particularly to infected and carrier animals. Salmonellae can survive for long periods in soil and manure.
- Autogenous bacterins have been used with variable success.
Public Health Significance
Salmonellosis is a zoonosis and special efforts should be made to avoid exposure to potential sources of salmonellae.
Sarcoid
This is the most common neoplasm of horses, mules, and donkeys, worldwide.
Cause
It is assumed but has not been proved that the cause is a virus. There is some evidence that bovine papillomavirus types 1 and 2 may be involved in the cause of sarcoid. This is mainly based on the demonstration of viral DNA sequences in sarcoid tissue, and the fact that experimental infection with these viruses in horses results in sarcoid-like lesions.
Transmission
There is evidence that sarcoids are transmissible by direct contact, arthropods and fomites.
Clinical Features
Most sarcoids occur on the extremities, ventral abdomen and head of equids less than four years of age. In general they are described as flat or raised, pedunculated or verrucous, hairless and firm and adherent to the underlying connective tissue. They vary greatly in appearance and as many as six different appearing types have been described. Location varies somewhat with geographic regions. In the US they are seen most frequently on the head, cervical region and head. Many animals will have multiple lesions. They vary in size from !-20cm. and may persist for years. They do not metastasize and rarely disappear spontaneously.
Diagnosis
- Diagnosis is usually based on the characteristic appearance.
- Definitive diagnosis requires histologic examination of a biopsy.
Figure 1a. One of several types of sarcoid.
Figure 1b. Fibroblastic sarcoid.
Treatment
- Excision and cryosurgery are preferred treatments; two freeze-thaw cycles are used. Recurrence is 30 - 50% after surgical removal.
- Immunotherapy using BCG vaccine or an extract of Mycobacterium bovis (commercial preparations are available); regression may take several months; the control rate is about 50%.
- Radiation therapy has a somewhat higher control rate than immunotherapy but is expensive and not widely available.
Sporotrichosis
Sporotrichosis is an infrequent chronic fungal disease of Equidae characterized by the formation of suppurative nodules mainly involving limbs.
Cause
The dimorphic fungus, Sporothrix schenckii which is present in soil and decaying wood and vegetation. The mycelial phase occurs in nature and the yeast phase in affected animals.
Occurrence
The disease occurs worldwide in many animals and humans.
Mode of Infection
The portal of entry of conidia is most commonly via cutaneous wounds of limbs. The latter have various causes including slivers, barbs and thorns. Disseminated disease due to the inhalation of the organism or spread from initial lesions is rare.
Clinical Features
The nodules (≈1 - 3 cm) which frequently suppurate involve mainly the skin, subcutis, superficial lymphatics and lymph nodes.
In horses, the infection often begins in the lower part of the leg and spreads upward via the lymphatics resulting in a chain of small, often suppurating, nodules. Ulcerating nodules exude a blood-tinged pus.
In the rare disseminated form there is hematogenous spread to vital organs, bones and CNS with a frequently fatal outcome.
Figure 2a. Nodules of sporotrichosis.
Figure 2b. Characteristic suppurating nodules of sporotrichosis.
Diagnosis
The disease in the horse and mule resembles in appearance ulcerative lymphangitis (Corynebacterium pseudotuberculosis) and epizootic lymphangitis (Histoplasma farciminosum). Nocardiosis, cutaneous glanders and mycetomas caused by various fungi are other diseases that should be considered. Laboratory confirmation should be sought.
Humans can readily be infected if infectious material enters the skin via cuts or abrasions.
- For direct examination: The cigar-shaped bodies that occur in lesions are very difficult to demonstrate in stained smears and wet mounts. Fluorescent antibody staining has increased the success of direct examination.
- For culture: The two phases of this dimorphic fungus can be readily cultured and identified; It takes from 1 - 3 weeks to grow.
Treatment
- Potassium and sodium iodide are used orally and intravenously; they are almost always effective.
- Oral organic iodide (EDDI) should be administered for a minimum of 1 month. Amphotericin B, flucytosine (5-fluorocytosine), and natamycin (pimaricin) have been effective. Ketoconazole, fluconazole, and itraconazole are effective. Treatment should be continued for a month after the infection appears to be cured.
Public Health Significance
As mentioned above humans can be readily infected if infectious materials enter wounds and the latter may not be evident. Veterinarians have been infected from horses. Great care must be taken while handling infected equids to avoid exposure. Associated personnel should be apprised of the risk.
Strangles
Strangles is an acute contagious, bacterial disease mainly of young equids characterized by rhinitis, pharyngitis and abscesses in dependent lymph nodes.
Cause
It is caused by the gram-positive bacterium, Streptococcus equi also referred to as Streptococcus equi subspecies equi.
Occurrence
This is a relatively common disease with worldwide distribution. Young horses are most commonly affected but all ages may be. Susceptibility is dependent on the animal's immune status.
Transmission
Infection is mainly by inhalation and spread may also be by contact and fomites.
The disease is usually acquired from carrier horses. This most often happens when horses from different locations are brought together, e.g., at shows, sales, polo-fields, and racetracks.
Clinical Signs
The incubation period is 3 - 14 days and the course 2 - 4 weeks with recovery.
Clinical signs include fever, anorexia, difficult swallowing, extension of head and neck and coughing. There is rhinitis and pharyngitis with later swelling and eventual abscessation of lymph nodes, particularly the intermandibular and parapharyngeal that drain the upper respiratory and buccal mucosa. The swelling may lead to suffocation ("strangles") with the need for emergency tracheotomy. There is profuse purulent nasal discharge. The abscessed lymph nodes rupture in I - 2 weeks discharging large amounts of pus.
A mild catarrhal form of strangles characterized by fever, nasal discharge and cough is seen in older horses with some immunity to S. equi.
Figure 3. Strangles: Submandibular swelling due to abscessation.
Among the infrequent sequelae are variably disseminated abscesses and purpura hemorrhagica (Type III hypersensitivity). Infrequently abscesses of the parapharyngeal lymph nodes rupture leading to infection of the guttural pouch and sinuses. Horses thus infected may become carriers.
In rare instances the disease may be generalized and terminate fatally. Bastard strangles is an infrequent chronic form with disseminated abscesses mainly in lymph nodes of the abdomen.
Diagnosis
A diagnosis is usually made on the basis of the characteristic clinical signs; however, laboratory confirmation is recommended
- Horses suffering from S. equi infection are at risk for developing complications. In severely affected individuals, upper airway endoscopy, thoracic ultrasonography and thoracic / skull radiographs may be indicated. Upper airway endoscopy is indicated for those individuals with severe nasal discharge. This evaluation will aid in identification of exudate and potential for chondroids allowing for facilitated lavage when necessary.
- Fresh pus for culture is taken on a swab from, preferably, an excised mature abscess. The isolation and identification of S. equi provides a definitive diagnosis. Older discharging abscesses may yield S. equisimilis, which is a secondary invader.
- A procedure is available to test for anti-M protein antibodies (IgG); it is referred to as the SeM protein test. This is particularly useful for those individuals at risk or showing signs of purpura hemorrhagica (PH). The serum titer will not rise immediately, so in acute cases the values may initially be low (<1:1600), with more severe disease or (in preparation) as a result* of vaccination high titers (> 1:1600) are obtained. In the absence of vaccination high titers indicate that PH may be present. Vaccination is contraindicated in individuals with high titers.
- PCR testing is available for nasal discharge or guttural pouch lavage samples.
Treatment
- Nursing care, complete rest, fluid therapy if indicated.
- Treatment with antimicrobial drugs is controversial. High doses of penicillin, sulfonamides, or trimethoprim-sulfadiazine for 7 - 10 days are recommended for severe cases and nursing foals. Persistent fever with pyemia is an infrequent complication for which the outlook is poor. If treatment is early the development of abscesses can be prevented or reduced.
- Surgical drainage may be indicated. Tracheostomy may be necessary.
Prevention
- Isolation and monitoring of horses to be added to a stable for 3 - 4 weeks.
- *Vaccination is only recommended for high-risk individuals, e.g. introduction to a farm with endemic strangles. Vaccination appears to reduce disease severity.
- Intranasal vaccine: Horses not previously vaccinated against Strep. equi subsp. equi should receive an initial series of 2 vaccines approximately 4 weeks apart. Annual boosters are recommended in high risk individuals.
- M-protein (subunit) vaccine: Adults should be vaccinated with an initial series of 3 vaccines at 4 week intervals with booster vaccination at 10 - 12 month intervals.
- Foals considered at high-risk should be vaccinated with an intranasal vaccine beginning at 6 months of age with an initial series of 3 vaccines administered at monthly intervals.
- Booster vaccines should be administered annually.
*Modified and reproduced with permission from Davis, E. Refresher on equine immunology and vaccines, DVM magazine, Fall, 2007.
Tetanus
Tetanus is an acute, non-contagious, neurotoxic disease of farm and other animals characterized by painful tonic and clonic spasms of skeletal muscles.
Cause
Clostridium tetani, a large, gram-positive, spore-forming, anaerobic rod. Its highly resistant spores are present in the soil and feces of animals. The organism is not more prevalent in horse manure, but horses sustain more wounds that allow for the growth of C. tetani.
Tetanospasmin or neurotoxin of C. tetani is one of the most powerful exotoxins known. It is a heat labile protein produced by proliferating cells and released during autolysis. This neurotoxin is responsible for the characteristic tonic and clonic spasms of skeletal muscles. Animal species vary in their susceptibility to the toxin and equids and humans are the most susceptible. One milligram of pure toxin contains ~100 million mouse lethal doses.
Toxin is elaborated at the site of infection and passes along the axis cylinders of the motor neurons of the medulla and spinal cord. It binds almost irreversibly to the gangliosides of nerve cells and thus antitoxin may not be effective. All isolates of C. tetani produce only one antigenic type of neurotoxin. The toxin acts at the inhibitory synapse where it blocks the normal function of the inhibitory transmitter. This results in excitation of the central nervous system as evidenced by hyperesthesia and the greater intensity of reflexes.
Occurrence
The disease is worldwide in distribution. Tetanus is seen in veterinary practice most commonly in horses and sheep. It is rare in dogs and cats. All ages are susceptible. Castration wounds, umbilical infection (tetanus neonatorum) and parturition (puerperal tetanus) are among the circumstances that can contribute to tetanus in animals.
Mode of Infection
The spores of C. tetani enter a variety of wounds and if necrosis is present they may germinate, grow and produce neurotoxin.
Spores may germinate in dirty and neglected wounds with some necrosis (lowered oxidation reduction potential=anaerobiosis) and when cells autolyse toxin is released at the site of infection.
Clinical Features
The incubation period is usually one to several weeks with an average about two weeks.
The first sign of tetanus to appear in horses is the inability to retract the nictitating membranes. This is followed by convulsive contractions of the muscles of the fore and hind limbs then other voluntary muscles. Characteristics of the disease in horses are erect ears, dilated anterior nares and stiff tail. Because of spasms of head muscles there is difficulty in prehension and mastication. There is general stiffness, marked hyperesthesia with more intense reflexes. The "sawhorse" stance is particularly characteristic of tetanus in foals. In fatal cases, muscles throughout the body become involved. When death ensues, it results from spastic paralysis of muscles facilitating respiration. In nonfatal tetanus, the spasms lessen and fewer muscles are involved. The fatality rate is ~80%
Figure 4. Saw-horse stance of foal with tetanus.
Diagnosis
Some features of tetanus are wounds (not always found, particularly in horses), gradual onset of stiffness, hyperesthesia, followed by tetanic spasms of all voluntary muscles. The fatality rate in horses without treatment is close to 100%. In contrast to tetanus, acute strychnine poisoning runs a course of one to several hours.
This disease is so characteristic clinically that a laboratory diagnosis is not required.
- If it is desired to attempt isolation and identification of C. tetani, material (pus, necrotic tissue) from the wound should be taken so as to minimize exposure to air (oxygen), preferably in an anaerobic transport system.
- Gram-stained smears from a wound may reveal the characteristic drumstick (terminal spore) bacteria; however, their absence does not exclude tetanus.
Treatment
- Expose, clean, and disinfect wounds.
- Muscle relaxants and sedatives. Stomach tube feeding. Dark, quiet environment.
- Penicillin and an adequate dose of tetanus antitoxin; intrathecal administration of antitoxin is used by some clinicians.
- With comprehensive treatment the fatality rate can be reduced.
Prevention
- To prevent tetanus in a wounded animal that has not been vaccinated or if the vaccine status is not known, clean and disinfect the wound. Administer antitoxin and toxoid at different locations; a large dose of penicillin may also be given. Toxoid is given again in 30 days. The potential for serum hepatitis exists following administration of tetanus antitoxin, so the antitoxin should only be administered to high risk individuals.
- For prevention, administer 3 doses of toxoid 3 - 6 weeks apart with a booster dose given annually.
- Foals at 6 months of age are given 3 doses of toxoid at 4 - 6 week intervals with an annual booster.
Tuberculosis
Tuberculosis is rare in horses. Most cases are caused by Mycobacterium avium. In a cutaneous form granulomas that may ulcerate are found on the upper limbs and abdomen.
In the generalized form tuberculous granulomas are found in various organs and tissues including lung, liver, kidney, lymph nodes, colon and myocardium.
There are reports of infection of cervical vertebrae by M. bovis.
Nodular granulomas involving the skin of legs have been attributed to several species of atypical mycobacteria.
Diagnosis
Tuberculosis in horses is most often diagnosed at necropsy.
- A highly presumptive diagnosis is usually based on the demonstration of typical acid-fast organisms in acid-fast stained smears from lesions. Smears of biopsies and exudates can likewise be stained for acid-fast organisms.
- Radiography may be helpful in diagnosis.
- Although culture may be carried out in a local diagnostic laboratory, definitive identification of mycobacteria may require the aid of a reference laboratory.
- The tuberculin test has not been reliable.
Treatment
- This is not considered advisable or feasible when the disease is generalized
- Surgical resection for granulomas of the skin.
Tularemia
Tularemia is primarily a bacterial disease of wild animals that is occasionally transmitted by various means to domestic animals including rarely the horse.
Cause
The cause is the small, gram-negative, facultative intracellular bacterium, Francisella tularensis which consists of two biotypes: the more virulent type A, referred to as tularensis, and the milder type paleartica. The biotypes differ in host specificity, biochemical activity, and geographical distribution.
Occurrence
The disease occurs in horses of all ages but is rare.
Biotype A tularensis occurs mainly in the northern hemisphere and is predominant in North America; biotype B, paleartica, is found in Eurasia.
Transmission
Wild animals are the reservoir of infection, especially rabbits and hares, but also beaver, muskrat, squirrel, woodchuck, opossum, skunk, deer, elk, bison, and fox. Domestic fowl can act as a reservoir of infection.
F. tularensis is most frequently transmitted by ticks but also by a large range of biting arthropods including flies, mites, mosquitoes and lice. Infection also takes place via aerosol and ingestion of contaminated food and water.
Clinical Features
The incubation period is usually less than 10 days. What begins as a localized infection proceeds by infection of macrophages and their spread to lymph nodes, liver, and spleen with formation of granulomatous, necrotic foci. Severity of the disease is variable depending upon the location and extent of lesions.
Among the clinical signs are fever, weakness, stiff gait, edema of limbs, anorexia, dyspnea and diarrhea, followed by prostration and frequently, death if untreated.
Diagnosis
A history of exposure to ticks that may have been feeding on a sick or dead wild animal could be suggestive. Although tularemia is rare in the horse it should be considered when a sporadic, severe, febrile infectious disease occurs.
If tularemia is suspected, great care should be taken in performing a necropsy. All work with material from suspected tularemia cases must be carried out in a biological safety cabinet or alternatively sent to a laboratory equipped to handle this highly infectious, dangerous organism.
- For serology: Serum samples are taken in the advanced disease and paired samples if obtainable. An agglutination test is usually positive late in the disease. A 4-fold increase in titer of paired sera is significant. An indirect fluorescence assay is also available to detect antibodies.
- Portions of liver, spleen, and lymph nodes with the characteristic necrotic foci provide material for smears and culture. This gram-negative organism, which somewhat resembles a Brucella species, requires a medium containing cysteine for growth. The most rapid means of identifying F. tularensis is by the specific fluorescent antibody staining of smears from biopsies and lesions. A slide agglutination test using known specific antisera is also available in some diagnostic laboratories to identify colonies of F. tularensis.
Treatment
- Streptomycin is the drug of choice; tetracyclines including doxycycline are also effective; prolonged treatment is necessary.
Prevention
- Little can be done other than attempt to reduce tick exposure.
Public Health Significance
Francisella tularensis causes a serious disease in humans. As mentioned above great care should be taken to avoid exposure to this highly infectious agent. Some laboratories decline to attempt culture.
Tyzzer’s Disease
Tyzzer's disease is a severe, usually fatal, bacterial infection of many animals including foals.
Cause
The cause is the large, spore-forming, motile, gram-positive, anaerobic rod, Clostridium piliformis which is part of the normal intestinal flora of many rodents.
The organism has not been cultivated in artificial media, but can be grown in cell cultures and in the yolk sac of chicken embryos.
Occurrence
The disease is probably worldwide in occurrence. It has been found in laboratory mice, rats, hamsters, gerbils, rabbits, nonhuman primates, horses, dogs, cats, and other animals. Although known for many years, it has only been reported in dogs, cats, and foals in recent years. The age range of susceptibility for foals is usually 1 - 5 weeks. Although usually sporadic there may be a cluster of cases on some farms. Adult horses may be carriers.
Mode of Infection
This by ingestion or arising from the affected individual’s own flora (endogenous). The disease is thought to possibly result from various stresses.
Clinical Signs
Foals may be found dead or in a coma without showing premonitory signs. The disease is characterized by enteritis (not in all cases), ileocolitis and focal, necrotic hepatitis.
Some foals may show depression and icterus and die within 24 hours. The course is about 48 hours. Clinical signs are only apparent for a short period; they include fever, icterus, and occasionally diarrhea. Recovery is rare.
Diagnosis
Acute salmonellosis, Actinobacillus equuli infection, and Rhodococcus equi septicemia (rare), and other acute microbial infections should be considered. There are no diagnostic procedures for definitive diagnosis in the live foal.
- For pathology and smears: Portions of the liver, fresh and fixed. The disease is usually diagnosed by finding the typical liver lesions (multifocal necrosis) and demonstrating the characteristic organisms in hepatocytes in stained smears. Liver sections stained by the silver impregnation method are also useful for the demonstration of the organism at the margin of lesions. As mentioned earlier the organism cannot be cultured in artificial media.
Treatment
- Treatment cannot ordinarily be instituted in time. If suspected large doses of penicillin or ampicillin may be given intravenously; however, if the individual has the disease it usually dies.
Prevention
- Improvement of sanitation if indicated; reduction of stresses.
- Clostridium piliformis produces spores that require a temperature of 80°C for 30 minutes for inactivation. Strict sanitary measures should be implemented to prevent spread to other foals.
Urinary Tract Infections
Urinary tract infection refers broadly to infection of the kidney, bladder, or urethra; more than one may be affected. Cystitis, which is relatively infrequent, is by far the most common urinary tract infection in the horse. Pyelonephritis occurs occasionally in postpartum mares.
Some characteristics of equine cystitis are as follows:
- Cystitis is more common in the mare.
- It may be secondary to urolithiasis.
- It is usually an ascending infection.
- In older mares cystitis may result from uterine or vaginal infections.
The bacteria most often involved are: Escherichia coli, Proteus mirabilis, Klebsiella spp., Enterobacter spp., Pseudomonas aeruginosa, Staphylococcus spp., Streptococcus spp., Corynebacterium renale.
There are frequent efforts to urinate that may be painful. The horse may continue to stand as though urinating, and strain to do so. Small amounts of urine are passed, and blood and pus may be present.
Diagnosis
Urine for culture should be collected by catheterization. See Section 4 for the handling of urine for submission to the diagnostic laboratory.
Treatment
- Treatment is indicated if the bacteriological examination indicates a bacteriuria.
- The drug to be used for treatment will depend on the antimicrobial susceptibility test. Among the drugs used are: trimethoprim-sulfadiazine, enrofloxacin, gentamicin, penicillin, ampicillin, amikacin, cephalosporins (3rd generation preferred), and tetracyclines.
- The efficacy of treatment is determined by a follow-up bacteriological examination.
Vesicular Stomatitis
Vesicular stomatitis is a contagious viral disease of cattle, horses, pigs, and goats, characterized mainly by the formation of vesicles, followed by erosions, of the mucous membrane of the mouth.
Cause
The cause is a rhabdovirus (Rhabdoviridae). The two important serotypes are designated New Jersey (most virulent and common) and Indiana. The latter type has three subtypes that occur in South America where there are endemic regions. The virus can remain viable in the environment for several days.
Occurrence
The disease occurs periodically in North (mainly southwestern USA), Central and South America. Recent outbreaks occurred in horses in Arizona, Colorado, New Mexico and Utah.
Horses, cattle, goats, swine and humans are susceptible, as are bighorn sheep, deer and antelope.
Transmission
The disease is spread rapidly by direct contact, biting insects, and fomites.
Clinical Features
The incubation period is usually 2 - 8 days.
Vesicles containing clear fluid are found involving the mucous membrane of the tongue particularly, the mouth and the coronary band. Lesions have been found less frequently on the nasopharynx, turbinates, larynx, prepuce and mammary gland. The vesicles swell, break and leave painful ulcers or erosions. Horses drool and are reluctant to eat and drink, and may display lameness. Most horses recover fully within a month.
Figure 5. Drooling characteristic of vesicular stomatitis.
Diagnosis
When horses sustain a vesicular disease with the characteristics of VS, one can almost be certain that it is VS in that the horse is not susceptible to foot-and-mouth disease, nor is it susceptible to swine vesicular disease and vesicular exanthema except that some viral strains of the latter rare disease can produce vesicles in horses.
In many countries, including the USA, vesicular stomatitis is a notifiable disease. Specimens will be collected by state, provincial, or federal animal health officials.
- Epithelial tissue covering the vesicles in the mouth should be collected and placed in buffered glycerol or frozen for shipment. If available, vesicular fluid should be collected aseptically in a sterile vial and frozen. Virus isolations are attempted. Tissue suspensions and vesicular fluid are tested for antigen using the ELISA, complement fixation (CF) or virus neutralization (VN) procedures. If virus or antigen is not detected material it is passed in mice, embryonated eggs or cell cultures, then retested.
- Paired serum samples (acute and convalescent), can be used for ELISA, CF, or VN tests to determine if there is a rise in vesicular stomatitis antibodies.
Treatment
- None, except the use of mild antiseptics and astringents on the mucosa of the mouth and provision of soft feed.
Prevention
- In many countries when a suspected vesicular disease occurs, it should be reported immediately to officials in charge of animal health.
- Affected animals are isolated and quarantine may be applied.
- After outbreaks premises are thoroughly cleaned and disinfected.
- Vaccines are employed in some countries in South America.
Public Health Significance
Humans can acquire the virus from infected horses. The infection in humans is influenza-like with stomatitis characterized by blisters in the mouth, fever, headache and general malaise.
West Nile Virus Infection*
The West Nile virus has a reservoir in birds and is transmitted by mosquitoes to horses in which it may produce a serious encephalitis.
Cause
West Nile virus is a flavivirus which belongs in the Japanese encephalitis serogroup of the family Flaviviridae.
Occurrence
West Nile virus infection (WNVI) occurs in countries of Asia, Africa, Europe and North America. The virus was introduced to the USA in 1999 and by 2004 it had spread throughout the continental USA. There were > 4000 human cases in 2002, with 274 deaths, mainly in people over 60 years of age. Less than 1% of those infected were symptomatic. The number of cases will probably decrease as the infection becomes endemic.
During the same period that human cases occurred there were many reports of the disease affecting horses in the USA. More than 15,000 cases were reported in 2002 and somewhat less in 2003. Older horses are more susceptible. It is estimated that 10 - 30% of the horses infected develop clinical disease.
In 1997 in Israel a neuroparalytic disease of young geese was attributed to WNV. Geese appear to be the only natural host among domestic avian species.
Transmission
This is mainly by mosquitoes. It is estimated that at least 58 mosquito species can carry the virus. Culex pipiens is considered the most important for maintaining the virus. Upwards of 300 bird species harbor the virus, many without evidence of clinical disease. House sparrows are thought to be the most important in dissemination. They are readily infected and have high levels of virus. Although some birds such as crows, blue jays and magpies may die of infection, house sparrows don’t.
Clinical & Pathologic Features
The incubation period in horses is 7 - 14 days. Signs may appear suddenly or gradually; they may include incoordination, dragging hooves, buckling at knees, difficulty eating and drinking, stumbling, muscle weakness, dullness, somnolence, paralysis, inability to rise. Some horses may have a mild infection with low fever, muscle trembling and evidence of a less severe disease.
Many horses that recover from the disease have residual abnormalities such as irregularities of gait, behavioral changes and neurological deficits six months after diagnosis. If horses don’t recover sufficiently they may have to be euthanized. The mortality rate in unvaccinated horses developing clinical disease is ~33%. Horses surviving infection are considered immune for life.
The lesions in horses are very similar to those of eastern equine encephalitis (EEE). There is perivascular lymphocyte cuffs, gliosis and neuronal degeneration. What is distinctive with West Nile infection is a poliomyelitis affecting the gray matter of the spinal cord. The brainstem and midbrain are also affected but not usually the cerebral cortex. In EEE the whole brain is affected with the cerebrum most affected.
Diagnosis
- Serum IgM with the capture ELISA is the preferred confirmatory diagnostic test.
- Clinical specimens: Whole blood collected during the febrile stage and brain tissue from horses that have died. Acute and convalescent sera.
- A presumptive diagnosis is often based on clinical signs and the microscopic brain lesions referred to above. It can also be made on the basis of clinical signs and results of a single serum sample, if those results are positive and the horse has not been vaccinated.
- A definitive diagnosis can also be obtained by demonstrating a significant increase in specific antibody between acute and convalescent sera.
- The virus can be propagated on the chorioallantoic membrane, where it produces plaques, and in various cell cultures.
Treatment
- Steroids to reduce inflammation; general supportive care. An equine product containing specific viral antibodies is being used in early treatment of non-vaccinated horses.
Prevention
- Vaccination is recommended. One inactivated vaccine is given in two doses 3 - 6 weeks apart. A recombinant vaccine using a canary poxvirus vector is also available. Two doses are given with annual boosters. A one dose, DNA vaccine (first of its kind licensed in the USA), claims to prevent viremia in WNV infection. Some practitioners vaccinate every four months with the inactivated product where mosquitoes are present year-round. The inactivated vaccine is considered safe for broodmares.
- A chimera vaccine (live, weakened yellow fever virus with genes from WNV) has been approved in the USA. An initial series of two doses is given with an annual booster,
- Strict mosquito control greatly reduces the chances of exposure. Keep horses indoors from dusk to dawn when insects are most active; keep lights off during the evening and keep stable areas clear of birds and poultry.
Public Health Significance
As stated above this virus can infect humans, sometimes seriously. Measures should be taken, including mosquito control, to protect personnel who might be exposed when the equine disease occurs or is suspected.
*Adapted from, A Concise Review of Veterinary Virology, Carter, G.R., Wise, D.J. and Flores, E.F. 2005, International Veterinary Information Service (Available from www.ivis.org).
Zygomycosis (Basidiobolomycosis, Conidiobolomycosis)
This rare mycosis, which mainly affects the nasal mucosa and subcutaneous tissue, is primarily a disease of horses although some other animals are occasionally affected.
The fungi involved, which occur in soil and decaying organic matter, belong to the genera Basidiobolus and Conidiobolus. Two of the principal species of these genera are mentioned below but other species can be involved.
Conidiobolus coronatus, which infects mainly the horse, produces ulcerative granulomatous lesions involving the mucous membrane of the nasal passages and mouth. Nasal discharge and mechanical blockage may result.
Lesions caused by B. ranarum may be large and involve the skin of the head, neck, and chest. There may be ulceration, yellow necrotic centers, fistulous tracts, with extension to regional lymph nodes.
Diagnosis
The nature and location of the lesions help distinguish zygomycosis from phaeohyphomycosis and cutaneous habronemiasis.
- Material (exudates, discharges) from lesions is examined for large, branching, occasionally septate hyphae. The same fungal elements are seen in stained sections of lesions.
- Exudates, discharges and fresh material from lesions are cultured. Because these fungi are widespread in nature and are often contaminants in specimens and on media, the finding of the fungal elements in tissue sections is especially significant. Some fungal cultures may have to be submitted to a reference laboratory for identification.
Treatment
- Surgical excision with amphotericin B given locally and systemically.
- Immunotherapy, by which particulate fungal material is injected intradermally, is thought to be beneficial.
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Affiliation of the authors at the time of publication
1Professor Emeritus of the Department of Medical Sciences and Pathobiology, Virginia-Maryland Regional College of Veterinary Medicine, Virginia Tech, Blacksburg, Virginia, USA. 2 Department of Clinical Sciences, College of Veterinary Medicine, Kansas State University, Manhattan, KS, USA.
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