Introduction

When you examine the taxonomic origins of this group, you will find that they are extremely diverse. The only characteristics that they have in common is that they don’t ferment glucose (sugars) and have a rod shape.

You will note that there are a number of diseases in the list, however only disease syndromes below will be discussed in any detail. They are:

1. Otitis externa/media in dogs with a special focus on Pseudomonas aeruginosa infections
2. Infectious eye disease in ruminants with a special focus on infectious bovine keratoconjunctivitis caused by Moraxella bovis and Moraxella bovoculi
3. Melioidosis caused by Burkholderia pseudomallei
4. Infectious endometritis in mares caused by a number of bacteria including Klebsiella pneumoniae, Pseudomonas aeruginosa, Streptococcus equi subsp. zooepidemicus and the exotic and notifiable agent Taylorella equigenitalum.

Diseases in animals caused by the non-fermentative Gram-negative bacteria

In the Gammaproteobacteria Division:

1. Pseudomonas aeruginosa, an environmental bacterium, is a common cause of antibiotic resistant opportunistic infections in animals. it is a common cause of chronic, recurrent otitis in dogs.
2. Acinetobacter spp. are multidrug resistant environmental bacteria implicated in nosocomial infections.
3. Moraxella spp. occurring naturally in nasal and conjunctival mucosae causes eye infections in livestock, including “pink eye” in cattle.
   State which of these diseases are notifiable and their current disease status in Australia
4. Francisella tularensis is the cause of tularaemia, a zoonotic disease contracted from rabbits and small rodents. It is rare in Australia and therefore will not be dealt with in any detail. It is a Notifiable Disease.

In the Alphaproteobacteria Division

1. Brucella species that are carried in the lymph nodes of host animals, are the most pathogenic. Diseases caused by this Genus are Notifiable in Australia. (Separate set of notes)
2. Bartonella species are found in the bloodstream of mammals and invertebrates causing valvular endocarditis and bacteraemias. Bartonella henselae is the cause of cat scratch fever, a zoonotic disease contracted from the bites and scratches of cats.

In the Betaproteobacteria Division:

1. Burkholderia mallei is the cause of glanders, an equine zoonosis not present in Australia. Glanders is a NOTIFIABLE DISEASE in Australia. Rare global disease.
2. Burkholderia pseudomomallei is the cause of melioidiosis, a disease endemic to this region and the Tropics.  (Important)
3. Bordetella bronchiseptica in mammals and B. avium in turkeys is the cause of upper respiratory tract infections and bronchopneumonia. It is part of the kennel cough syndrome in dogs.
4. Taylorella equigenitalis is a NOTIFIABLE venereal disease of mares known as contagious equine metritis (CEM). It is absent from Australia.
5. Neisseria species found as commensals in the upper respiratory tract can cause opportunistic infections in animals. Won’t be taught.

THE FCB division of bacteria contains most of the gram-negative obligate anaerobic bacteria. However, in this group are also the aerobic, non-fermentative fish bacteria. Included is:

1. Flavobacterium columnaris the agent of columnaris disease, a gill and skin disease of farmed fish.
2. Tenacibaculum maritimum is a kidney commensal of marine fish that causes skin disease and tissue necrosis. It is a huge threat to the global marine fishing industry

The list of the more important diseases of animals (excluding Brucella  – in the following chapter) is shown in the Table below.

Tularaemia (rare zoonosis)

(I will rarely ask questions on this disease and if I do, it will not be for many marks)

Francisella tularensis, the cause of tularaemia, is a facultative intracellular gram-negative cocco-bacillus known to infect numerous animal species, including humans, and is a category A bioterrorism agent. F. tularensis subsp. tularensis) or type A (only USA – about 125 human cases per annum) which causes life-threatening disease and the less pathogenic F. tularensis subsp haloartica  are only found in the Northern hemisphere. The least pathogenic F. tularensis subsp. novicida and F. tularensis subsp. mediasiatica has a global distribution. To date there have been 2 human cases in Tasmania and one in NSW, all from the bites of ring-tailed possums and a case in Northern Territory which is thought to be water-associated. Australian cases have suffered from ulceroglandular tularaemia.

Transmission of the agent is from infected animals (rabbits, cats, rodents) either via aerosol (i.e. contaminated grass clippings), insect bites or other skin wounds (i.e. when skinning infected animal carcasses). The most common clinical presentations in humans are respiratory disease, lymphadenopathy (localised) and a systemic febrile illness. Symptoms generally show up 3 to 5 days after exposure, but sometimes as late as 14 days later. Symptoms in humans vary and include sudden fever, chills, headache, diarrhoea, muscle aches, joint pain, dry cough, swollen lymph nodes, skin ulcers, progressive weakness and pneumonia. Pneumonic tularemia can cause a severe and fatal pneumonia when the organism is spread by aerosol, as might occur in a biological attack. Humans are usually treated with streptomycin, ciprofloxacin, gentamicin or doxycycline.

Pseudomonas aeruginosa infections including otitis in dogs

Pseudomonas aeruginosa is a ubiquitous freshwater gram-negative motile rod that infects wounds and damaged tissue. It forms biofilms both in the environment i.e. water pipes and on tissue.  It is ubiquitous in watery environments. Although it grows aerobically, it can tolerate anaerobic conditions. This bacterium usually produces a green pigment known as pyoverdin, occasionally a brown melanin pigment known as pyomelanin, and  ketones that give it an apple cider-like odour. These characteristics will assist you in rapidly identifying its presence in tissue. This bacterium is intrinsically resistant to commonly used antibiotics and is often the reason why there is poor response to antibiotic therapy in some infections.

It most often infects burn wounds and surgical sites. You will encounter this bacterium regularly in veterinary practice as it is the most common cause of chronic canine otitis externa, endometritis in mares and surgical site infections. It should always be included in the differential diagnosis list in veterinary hospitals where there is an apparent outbreak of nosocomial infections.

Due to its wide temperature tolerance, it can infect a very wide host range. During wet conditions, it can cause a mild dermatitis and fleece discolouration in woolly sheep.

Antibiotics known to be effective include the fluoroquinolones, aminoglycosides, antipseudomonad beta-lactam drugs like ticarcillin and carbapenems and polymixin B. Resistance develops very rapidly to the fluoroquinolones.

An unusual case in Tasmania with devastating consequences

The orange-bellied parrots (Neophema chryogaster) are one of the most threatened parrot species in the world with less than 20 mating females in the wild. Thus it is important that captive breeding programs maintain and build up healthy stock for release into the wild. During one season 16 of these birds died from Pseudomonas aeruginosa septicaemia. The reason for this was that the feed seeds had been sprouted in a disinfectant that the P. aeruginosa was resistant to, allowing this bacterium to overgrow in the seed sprouts.

infectious keratoconjunctivitis in ruminants

Moraxella bovis is the primary cause of the highly contagious disease called infectious bovine keratoconjunctivitis (IBK), also known as Pinkeye or Forest Eye. This disease costs the Australian beef industry 13.3 million Australian dollars annually. This bacterium is rapidly spread throughout a herd of cattle in the summer time by flies (Australian bush fly, domestic fly), or direct contact with of ocular or nasal discharges. Note that different regions of the world will have different vectors. Up to 80% of a herd can become infected.  Long grass blades, thistles and seeds can cause microtrauma to the eye. Sunlight and dust exacerbates the disease. IBK is more severe in calves and cattle with non-pigmented skin around the eye i.e. Herefords.  The presence of other eye pathogens such as infectious bovine rhinotracheitis (BHV-1), Moraxella bovoculi, Mesomycoplasma bovoculi and Mycoplasmopsis bovis or a vitamin A and selenium deficiency will also increase the severity of the disease. It is a common disease in dairy cattle, feedlot cattle and cattle that are live exported.

In sheep and goats Chlamydia pecorum and Mesomycoplasma conjunctivae are the two primary causes, with a similar epidemiology to IBK.

M. bovis has two fimbrial types quick pili that assist the bacterium in colonization of the cornea and intermediate pili that maintain adhesion of the bacteria to the cornea.  These fimbriae preferentially bind to dark (aged) corneal cells. Intense UV light increases the numbers of dark corneal cells and corneal defects. Moraxella bovis also produces haemolysins (RTX cytotoxins) that work by porin formation that erode the cornea and provide a portal of entry into the eye by the bacteria. There are 7 antigenically unrelated serotypes of M. bovis and the fimbriae can vary antigenically. Thus current commercial vaccines whilst very effective against homologous strains of M. bovis tend to be less effective in the field where there are a number of different antigenic types of M. bovis present.

IBK is suspected when there are conjunctivitis and keratitis in high numbers of intensively reared cattle, mainly calves, in a herd usually during the summer months. 10% of more of the cattle will develop corneal ulceration. These cattle also show aversion to sunlight and will cluster in shade. Only the eye is affected, which helps distinguish this disease from other causes that also affect the respiratory tract e.g. bovine rhinopneumonitis.

An early diagnosis when the eye has liquid tears, the conjunctiva is red and there is a slight cloudiness to the eye with a circular area on the cornea indicating an early ulcer. Fluorescein in the eye can assist you in determining whether an ulcer is present and the depth of the ulcer (clear margins the ulcer is superficial, fuzzy margins the ulcer is deep). If not treated the ulcer could become full thickness and allow the eye contents to extrude. When this happens the prognosis for a full recovery or the eye is poor. Reddening of the corneal ulcer indicates that healing with neovascularisation is occurring. Whiteness of the ulcer without much lacrimation indicates that healing is occurring with scar formation. Furthermore, scars don’t take up fluoroscein dye.

The diagnosis is confirmed by culture and identification of Moraxella bovis. A multiplex PCR can identify M. bovis, M. bovoculi, Mycoplasmopsis bovis and BHV-1.

Mild IBK if the lesions are less than 5 mm in diameter can heal spontaneously. If there is concern they can be treated with cloxacillin eye ointment. (The concentration of cloxacillin in intramammary preparations is generally too low to be effective). More advanced cases with parenteral oxytetracycline or other effective antibiotics like florfenicol or tularithromycin.  Subconjunctival injection of antibiotics may be effective, but there is no proof that this method is more effective than parenteral administration of antibiotics. In addition to the parenteral and local antibiotic therapy an eye patch is used to protect the eye. A denim or other type of patch is glued in place over the affected eye. In severe cases, the eye can be sutured closed (tarsorrhaphy) or third eyelid or conjunctival flaps will protect the eye. Topical atropine ointment applied 1 to 3 times a day will reduce ciliary body spasms and pain. Keep treated animals in the shade. NSAIDS can also be used to reduce inflammation and pain.

Prevention is by vaccination administered 3 to 6 weeks before the onset of summer or when the prevalence of pink-eye is high.  This is usually when there is a lot of dust and the fly numbers are high. Note that due to strain differences of M. bovis, antigenic variation in the pili antigens means that the vaccine won’t be effective on all farms. In these cases you might choose to use an autogenous vaccine. Furthermore vaccines that contain a lot of different strains may not be that effective due to antigenic competition. Despite the variation in response to the vaccines, most farms that use it claim to have a reduction in pink-eye in cattle. Note that there is no pink eye vaccine for sheep and goats.

Essential too it the control of diseases and plants (dry thistles) that exacerbate the lesions, good fly and dust control, the provision of shade and improving the nutrition status of the animals.

Burkholderia pseudomallei and B. mallei the agents of melioidosis and glanders respectively

Members of the genus, Burkholderia used to belong to the genus Pseudomonas i.e. they are aerobic, non-haemolytic and non-fermentative. Two important agents are recognised.

• Burkholderia mallei, the agent of glanders, an obligate pathogen of equids and a ZOONOSIS; and
• Burkholderia pseudomallei, the agent of melioidiosis, a soil and freshwater inhabitant that is found especially in the tropics

A common soil inhabitant that rarely causes wound infections is the Burkholderia cepacia group (they often produce yellow pigment).

Melioidosis caused by burkholderia pseudomallei

Burkholderia pseudomallei  (formerly Pseudomonas pseudomallei) is a gram-negative, bipolar staining, aerobic, motile rod-shaped bacterium. It is a BSL-3 bacterium. It infects humans and animals and causes a chronic granulomatous disease of the skin, respiratory tract,  and other internal organs known as melioidosis. The disease is endemic to the Tropics of central and South America, Central Africa, SE Asia and Tropical Northern Australia including Townsville and Cairns. It is a Bioterrorism category B threat.

Epidemiology of melioidosis

All species of mammals and parrots are susceptible to infection. Camelids, including alpacas, goats, parrots and koalas are especially susceptible to the disease. Sporadic animal cases have also been reported in Australia. Cases are more common in the warm, rainy season when the bacteria that usually live at a depth of 30 to 60 cm of soil (rhizoid layer) are brought to the surface by water run-off, flooding and soil excavation. Thus the bacterium will accumulate in rain washed soils in lower lying areas. In Townsville, the cases numbers occur from January through to March with a larger numbers of cases after flooding. It is able to infect and survive in soil-living  amoeba and roots of plants which could be why it easily adapts to an intracellular lifestyle in an animal or human.

Pathogenesis

Burkholderia pseudomallei enters the body of animals via the respiratory, oral and per-cutaneous routes. Once in the body, B. pseudomallei  attaches to macrophages and other cells and enters them by causing changes within the actin cytoskeleton through a T3SS effector (see salmonellosis). This allows it to be phagocytosed by macrophages and other cells as well as escape from the phagolysosome into the cytoplasm. It replicates in the cell cytoplasm without stimulating a bacteriocidal response. Either it will exit the cells by cell lysis or it moves from cell to cell using an actin tail (much like Listeria does). The latter form of spread results in cells fusing with the formation of multinucleate giant cells. It produces a number of virulence factors with one being an exotoxin known as Burkholderia lethal factor 1 (BLF-1) which causes cell necrosis by preventing ribosomes from manufacturing proteins. Surface antigens on B. pseudomallei will stimulate the recruitment of leucocytes to the site of infection and result in B. pseudomallei specific antibody production.  The picture below represents the cellular pathogenesis of B. pseudomallei.

The bacterium in more resistant animals will cause lesions at the site of entry, but not spread further. In more susceptible animals it will spread haematogenously to infect other organs including the spleen, liver and reproductive tract.

For more details on the pathogenesis of melioidiosis refer to this review (This is for information only and to assist you in understanding the pathogenesis – you only have to know what is in these notes):

Wiersinga WJ, Virk HS, Torres AG, Currie BJ, Peacock SJ, Dance DAB, Limmathurotsakul D (2018). Melioidosis. Nature Reviews Disease Primers volume 4, Article number: 17107

Diagnosis of melioidosis

The presence of multifocal abscesses/granulomas in various organs on post-mortem examination in endemic areas provides a high index of suspicion. Intracellular gram-negative rods are present in affected tissues. The bacterium grows rapidly on common laboratory media including blood and MacConkey agars. A specific selective agar that contains the antibiotics colistin (polymixin E, and gentamicin) known as Ashdown’s medium is used to grow it from contaminated specimens. The identification of this bacterium is confirmed by DNA specific PCR probes.

Animals can be screened for exposure to B. pseudomallei using serology.

Treatment and Control

B. pseudomallei is resistant to a number of antibiotics including gentamicin and colistin, but it is susceptible to amoxicillin plus clavulanic acid. The mechanism of resistance to the beta-lactams is by the use of efflux pumps. This is opposite to Pseudomonas aeruginosa, another highly resistant gram-negative bacterium. The recommended management for all forms of melioidosis in humans consists of an intensive phase of intravenous antimicrobial agents (such as, ceftazidime or a carbapenem) for a minimum of 10-14 days, followed by a prolonged course (3 months or longer) of an oral antimicrobial agent (such as, trimethoprim/sulfamethoxazole) to prevent relapse.

Because of the danger of laboratory-acquired melioidosis, this organism should be handled by trained personnel within a Biosafety Level 3 (BSL-3) facility when processing clinical isolates. The bacterium can be destroyed by heating about 74°C for 10 minutes, by UV radiation and 2% glutaraldehyde. Standard concentrations of chloride may not destroy all bacteria.

Since there are no vaccines available – prevention of melioidosis should be directed towards reducing contact of susceptible animals with the bacterium during high risk periods. Thus for goats where there is a possibility that the bacterium can be shed in the milk, it is important that they are fed off the ground during heavy rains and placed on above ground flooring. Animals can also be moved to higher paddocks that are not subject to water run-off.

Disease in humans

It is a notifiable disease in people. Most human cases have been reported in Northern Territory i.e. in 2012, 97 cases of melioidosis were reported during the wet season with 9 being fatal. Secondly is Northern Queensland.  Note that the recent floods in Townsville resulted in 12 human cases, 2 of which were fatal. (A link is provided to the Facebook page of 7 News, indicating just how serious the media were taking human infections with B. pseudomallei). Serious disease usually occurs in immune-compromised people i.e. diabetics, alcoholics or persons with renal and liver disease. Worldwide there are about 165 000 new cases each year with 89 000 of them fatal = about 50% fatality.

Not a zoonosis, as both humans and animals are infected from the soil reservoir. Only 3 possible cases of animal-associated melioidosis have been reported in Australia.

The incubation period of acute disease is 1 – 21 days, chronic disease is longer and some infections can remain latent only to occur when the patient become immune compromised. The clinical signs in people are unspecific and thus the disease must be suspected if within the incubation period after a flooding event in endemic areas.

Percutaneous infection usually results in localised ulcerative, suppurative granulomas; whereas inhalation of bacteria results in chronic bronchopneumonia. Ingestion of the bacteria can lead to infection of the lymphatic tissue of the oral cavity and pharynx. Both forms can result in haematogenous spread leading to septicaemia or multiple abscessation in a variety of tissues i.e. the skin, lung, liver and spleen. This form, even with treatment, has a case fatality rate of 40 to 50%.   If the patient is not treated it is up to 95%. A severe, acute form of the disease can result in acute respiratory distress syndrome (ARDS) which together with pneumonia can lead to respiratory failure. This is believed to be the result of the interaction between this intracellular bacterium and the immune system.

Treatment is usually with intravenous ceftazidime, a third generation, antipseudomonad cephalosporin followed by long-term potentiated sulphonamides.

In USA in 2021, an aromatherapy room spray manufactured in India was the source of B. pseudomallei for 4 patients that developed pneumonia a person was also infected via  freshwater aquarium that held tropical fish from South Asia..

Glanders (Notifiable disease, not present in Australia; Zoonosis)

This is a rare disease globally, so the risk of introduction of it into Australia is highly unlikely. However, if it were to be introduced it may be mistaken for melioidiosis.

So only learn the cause, what it does, how is it diagnosed and that it is notifiable

Glanders is a highly transmissible and fatal bacterial disease of horses, donkeys, and mules caused the bacterium Burkholderia mallei. The disease causes nodules and ulcerations in the upper respiratory tract and lungs. The skin form is known as “farcy”. While glanders primarily affects equids, it can also occur in dogs and other canids, cats and other felids, goats, camels, guinea pigs, hamsters and humans (It is a zoonosis). Cattle and pigs are resistant to disease. Carnivores are usually infected by eating contaminated meat.

It is a notifiable disease that is not present in Australia, but is endemic to parts of Russia, Mongolia, China, India, Pakistan, SE Asia and the Middle East. The latest cases are in India (February 2025). The disease is absent from most other parts of the world.

Burkholderia mallei is a slow-growing (requires 72 hours) fastidious, non-motile gram-negative rod. Horses contract glanders by close contact with other infected horses, especially through shared water and feed troughs as well as by nuzzling (direct contact). The bacteria can also be spread by fomites (non-living objects contaminated by infected animals), such as brushes, halters, or harnesses.

In equids the disease has a 1 to 2 week incubation period. The commonest sign of infection in animals is yellow-green nasal discharge and ulcers on the nose. The horse may have enlarged lymph nodes and nodules on the skin. In some cases, they may look like long, hard ropes, under the skin. Severe coughing can also occur. Animals and humans may die is not treated early. Long term infections can occur in horses, which may last for several years.

The disease is usually occupational in humans with infection by contact with infected animals where the bacterium is inhaled or enters via damaged skin or nasal and oral mucosa. The clinical signs are similar to melioidiosis.

Glanders in horses can be easily confused with melioidosis and other causes of skin nodules. Thus its presence should be confirmed by culture and qPCR and serologically (Complement fixation test). Due to welfare concerns, the mallein eyelid intradermal test is no longer recommended. However, it is still sometimes used in remote regions where laboratory testing is not possible.

Control is usually by the detection and euthanasia of positive animals and the materials they have been in contact with. Quarantine and limiting the movement of horses and not holding equine events in affected areas will limit the spread of glanders. In endemic areas antibiotics can be used which will decrease the clinical signs but not eliminate the bacterium.

Bordetella

Bordetella is a non-fermentative, gram-negative, motile coccobacillus that is usually susceptible to tetracyclines and is a commensal of the upper respiratory tract of animals. Bordetella bronchiseptica can cause upper and lower respiratory tract disease in animals and people. It is more often recognised as a cause of disease in dogs as part of the kennel cough syndrome, cattery cats and commercial pigs.

Bordetella avium is the cause of turkey coryza/avian bordetellosis and Bordetella pertussis whooping cough in people. To find out more on avian bordetellosis, refer to this on-line review. Jackwood, MW, Overview of Bordetellosis in Poultry (Turkey coryza, Bordetella avium rhinotracheitis). MSD manual, veterinary manual. I will not be teaching this disease.

Bordetella  bronchiseptica is a cause of a contagious tracheobronchitis in dogs (one of the important causes of ‘kennel cough’), cats, pigs, rabbits and occasionally humans. The disease is transmitted by the saliva and nasal secretions of infected animals. The bacterium can survive for up to 1 to 2 weeks in a moist environment and has been known to spread via air-conditioning. The disease of most often contracted when animals are kept in large groups i.e. animal shelters, pet shops, grooming parlours, kennels, catteries and large hospitals. Intensive rearing of livestock is a risk factor. Co-infection with respiratory viruses or other bacteria increases the animal’s susceptibility to disease i.e. kennel cough in dogs and atrophic rhinitis in pigs.

The incubation period is usually 7 – 21 days. Bordetella bronchiseptica colonises the upper respiratory tract and descends to the lower respiratory tract by attaching to the respiratory cilia and causing ciliastasis. The infection in most animals is usually mild with a mild fever, sneezing, a dry hacking cough and watery nasal discharge. Young and immune-compromised animals may develop a bronchopneumonia.

The disease is diagnosed on culture of swabs from the pharynx or better still and TTW (transtracheal wash) or BAL (bronchoalveolar lavage). qPCR can also be done on these swabs or after an overnight enrichment culture.

Mild cases can be treated symptomatically and usually don’t require antibiotic therapy. However, dogs or cats with a fever, lack of appetite and with signs of pneumonia should be treated with antibiotics. The bacterium is usually susceptible to antibiotics such as doxycycline and enrofloxacin. Walking dogs on a harness will decrease trachea irritation and hence coughing fits.

Risk of infection can be minimised by:

1. Keeping animals individually or in small groups
2. Isolating any animals that have evidence of infection
3. Dogs: Intranasal or SC vaccination with a live modified (intranasal/oral) or bacterin (parenteral) vaccine a week prior to being in groups. Note that immunity is of short duration. It is a non-core vaccine for dogs in Australia. However, some boarding kennels may request that dogs are vaccinated against B. bronchiseptica before they accept them as borders.

Below is a list of vaccines that can be used to prevent bordetellosis in dogs in Australia. No need to learn it.

infectious endometritis in mares

Bacterial endometritis in mares can result in infertility and abortion. It is a common condition globally. The most common agents causing bacterial endometritis are:

1. Streptococcus equi subsp. zooepidemicus
2. Escherichia coli
3. Klebsiella pneumoniae (capsular types 2 and 7)
4. Pseudomonas aeruginosa 

Less common, but leading to outbreaks of endometritis in mares is the gram-negative, non-fermenting and highly fastidious bacterium known as Taylorella equigenitalis. This is the agent of contagious equine metritis (CEM). This bacterium is absent from Australia and is a notifiable disease.

All the bacteria mentioned above, can either move via ascending infection into the uterus or be deposited in the anterior vagina by venereal transmission. Thus in outbreaks of infections on breeding farms, it is not only important to test the mares but also the stallions for infectious agents.

Even if the infectious agents are present, not all mares will develop endometritis. In the case of CEM which is the most contagious agent it is only 30 – 40% of mares served to a carrier stallion. Critical to disease is the presence of an open cervix and anatomical defects within the perineal area allowing gaping of the vulva lips and even wind sucking or urine pooling in the vagina. This happens as mare age or have poor back conformation.

When bacteria enter the endometrium they attach to the epithelium and grow and produce toxins. These stimulate a superficial endometritis with increased fluid in the uterus. This fluid can be detected by ultrasound. Pus develops 2 to 10 days post-mating which can leak out of the uterus and is observed as a purulent or mucopurulent vaginal discharge = dirty mares (sticky discharge that clings to the tail).  This leads to failure to conceive, embryonal reabsorption and occasionally an early abortion.

IMG_5973

Sampling for contagious equine metritis (CEM)

Contagious equine metritis (CEM) has a limited distribution globally as can be seen from the map below and many countries have been able to rapidly control any incursions. The disease was first reported in 1977 in the UK and had entered Australia in 1980, but was rapidly eliminated from both countries. It is a notifiable disease in Australia. To find out details on the requirements for the importations of horses, stallion semen and mare embryos. Refer to the Ausvet Plan on emergency animal diseases Response Policy Briefs Version 3.6, 2018 p18-19. (It is a category 4 disease that  will cause production losses affecting the equine breeding industry so the government will cover 20% and industry 80% of the costs of control).

Diagnosis of CEM is based on the culture from swabs with the identification done using T. equigenitalis-specific DNA probes. Samples are collected from the endometrium in clinically affected mares and from the external genitalia of mares and stallions to detect carrier horses. This is a very fastidious bacterium, so any swabs that have been collected should be immediately placed in Amies charcoal transport medium and reach the State veterinary laboratory on ice within 48 hours of collection. Best if it reaches the laboratory within 2 to 4 hours.

Note that endometrial swabs in Amies charcoal medium can also be used to culture the other bacterial pathogens of the uterus. In this case, you can use any veterinary laboratory.

Clotted blood (serum) can be collected for the Complement fixation test. It remains positive 3 to 6 weeks post-infection.

To detect carrier horses, specific sampling sites should be used:

• Mares in oestrous: 3 swabs – clitoral sinus; clitoral fossa and cervix. Demonstrating sampling of the mare is a YouTube video made by The Horse and Dr Tom Riddle.
• Stallions: 3 swabs – anterior urethra, urethral fossa and diverticulum and sheat/prepuce. Additionally, pre-ejaculatory fluid can be collected. YouTube video on the collection of samples from the stallion in shown in this YouTube video made by The Horse and Dr Pete Sheering.

Avoid pooling the swabs, as the samples can be heavily contaminated with normal mucosal microflora. 3 negative tests collected at weekly intervals are required for an animal to demonstrate freedom from T. equigenitalis. All imported horses, semen and embryos should have been tested negative for CEM before entering Australia.

Control of Contagious equine metritis (CEM)

Although it would be best to eradicate the causative agent immediately, it is recognised that if the bacterium is introduced into Australia, it may only be detected after being in the country for a while, thus a control then eradication programme is carried out.

Thus the aim will be on infected properties:

1. Stop any breeding activities
2. Quarantine and movement control on infected and exposed horses
3. Decontamination of infected facilities
4. Tracing to determine source and spread of the agent
5. Testing and treatment of infected horses until clear of the agent
6. Public awareness campaign

Rat Bite Fever (zoonosis)

Rat bite fever is a  rare septic disease in people resulting from the bites of rats and sometimes mice. Streptobacillus moniliformis (havermill fever) and Spirillum minus (sodoku) are the causative bacteria of this zoonosis. Infections with S. moniliformis are reported more commonly in the USA and S. minus in parts of Asia and Australia, mainly Japan. People are treated with intravenous penecillin followed by oral penicillins or aminopenecillins.

END OF CHAPTER