introduction

Compared to viruses and major protozoal diseases, very few bacteria are transmitted by invertebrate vectors. In this section, only those bacteria that rely entirely on invertebrate vectors for transmission will be covered. Those bacteria like Moraxella bovis, Bacillus anthracis and Coxiella burnettii that can be vector-borne, but also have a number of other means of transmission to their host will be covered in their respective sections.

Canine monocytic erhlichiosis (CME) or tropical pancytopaenia in dogs

Erhlichia canis is tick-borne intracellular rickettsial bacterium that infects mononuclear cells of the immune system causing fever, thrombocytopaenia, lameness and immune-suppression in canids.  For detailed information on the disease, read this short article written by Peter Irwin and John Beadle.

Guidelines on how to manage CME in Australia

Epidemiology

Geographical distribution in Australia

First detected in dogs in May 2020 at Halls Creek Western Australia. The distribution and locations of early reported erhlichiosis cases are shown in the map below.

Transmission and Spread

1. Vector: Brown dog tick Rhipicephalus sanguineus. (Refer to parasitology notes). This one-host (occasionally multi-host), hard tick is found world-wide, except in the UK, where its preferred host the dog is present. This tick thrives in warm climates and indoors. All life stages of the tick can carry E. canis and the bacterium can be transmitted intrastadially. However, the female does not pass the bacteria into her eggs (no transovarial transmission). Erhlichia canis is transmitted within 3 hours (rapidly) of the tick attaching to a susceptible dog. This tick is also host to other important bacterial and protozoal parasites of dogs, including Mycoplasma hemocanis, Coxiella burnetti, Babesia canis, Babesia vogeli and Hepatozoon canis. In information only – This article describes the biology of Rhipicephalus sanguineus.

2. Blood transfusions. Dogs can carry E. canis in the mononuclear cells of the blood without displaying clinical signs (sub-clinical carrier)

The agent is often spread by human-assisted dog movement. Note that sub-clinically affected dogs can harbour E. canis for a long time and some will breakdown and suffer from chronic disease months to years after infection.

Pathogenesis and clinical signs

The rickettsial bacterium is inoculated into the bloodstream by an infected tick and then ingested by circulating monocytes. Once in a phagocytic vesicle, it will absorb nutrients from the cell and replicate forming  a morula. These morulae can be recognised in the peripheral blood of infected dogs. Rickettsial parasites are unable to manufacture LPS or peptidoglycan for an outer membrane. This is probably one of the reasons why immune recognition of them is delayed. Another is that they show phase variation of their membrane proteins.

Infected bacteria will then circulate throughout the body infecting more mononuclear immune cells and lodging at various tissue locations. Clinical signs of acute disease take 1 to 3 weeks to develop. Infected cells are often trapped in lymph nodes resulting in a lymphadenopathy with swollen lymph nodes. An autoimmune response to the bacterium exacerbates the clinical signs often resulting in the production of platelet autoantibodies and lymphocytic accumulations in various tissues including the joints and eyes.

Thus clinical signs in acute disease lasts 2 to 4 weeks and are non-specific, but include:

• Fever, anorexia and lethargy
• Enlarged lymph nodes and spleen
• Thrombocytopaenia with a bleeding tendency hence petechiae and ecchymoses
• Non-regenerative anaemia
• Polyarthritis and polymyositis
• Intraocular lesions
• immune-complex glomerular nephritis

Some dogs will recover from the acute phase and some may never show the acute phase but become subclinically infected. These dogs may have a mild thrombocytopaenia. The bacteria of often sequested in the mononuclear cells of the spleen during this period that has been known to last up to 3 years in some dogs.

Some dogs will progress to the more severe chronic form of the disease. In this form all the clinical signs of acute disease are present, but more severe. Additionally the dogs show neurological signs and have pancytopaenia due to hypoplasia of the bone marrow. They are immune-suppressed and prone to secondary bacterial and protozoal infections. The prognosis of dogs with pancytopaenia is grave.

Diagnosis

1. Haematology and biochemical profiles. Important characteristic to alert one is a thrombocytopaenia

2. The presence of morulae in the cytoplasm of monocytes in the blood and macrophages. This is only observed in acute disease, so has a low sensitivity. Several peripheral blood smears may have to be examined before they are observed. However, this may be the first hint that the dog is suffering from erhlichiosis in non-endemic areas.

2. E. canis specific DNA in blood collected in EDTA. This test can also be carried out on lymph node aspirates, heart blood and affected organs. It is the most sensitive and specific of the tests.

3. Serum antibodies to E. canis using the immunofluorescence test. Not positive in early disease and antibodies can persist even if the infection has been resolved. A negative test has been used as an importation requirement for dogs into Australia. Note that this test can cross-react with other Erhlichia species such as E. platys a milder disease of platelets.

Control

Infection of dogs is prevented by effective tick control programs, including the use of environmental tick control, repel-and-kill tick products, regular coat examination for ticks and avoidance of tick infested areas. (Refer to parasitology notes).

There is no registered vaccine in Australia

Infected dogs should be restricted in their movement and should be treated with effective antibiotics such as doxycycline. Doxycycline is effective in the treatment of acute disease with clinical signs improving in 48 to 72 hours after the start of treatment. Treatment should continue for a minimum of 3 weeks to avoid these dogs becoming carriers. Euthanasia should be considered in severally affected dogs. Rifampicin can be used in cases where there is doxycycline is ineffective.

Borrelia species infections

A list of the more common diseases caused by Borrelia species is shown in the Table below.

Borrelia spp.  are tick-borne  blood parasites found in humans and animals. Their cell wall is rich in lipoproteins but lacks LPS. Unlike other bacteria, Borrelia has no need of iron, but rather uses manganese or other metals in its enzymatic processes. They grow under microaerophilic conditions in complex liquid or semi-solid media.

lyme’s disease

Lyme’s disease is caused primarily by Borrelia burgdorferi which is transmitted by Ixodes species of ticks. Although several animals species can be infected with this bacterium clinical signs are rare. This systemic disease can cause a variety of clinical signs. However, In dogs the most common clinical signs are lethargy, fever, a shifting lameness (joint inflammation) and swollen superficial lymph nodes (lymphadenopathy). In horses neurological signs are the most common. Since Borrelia burgdorferi is not present in Australia as  well as predominantly a human disease, you only need to know its name and the disease it causes.

Lyme’s disease is more common in people where a “bull’s eye” rash often develops at the tick bite site followed a few days later by flu-like symptoms. Chronic disease can develop which results in intermittent episodes of joint pain, myocarditis, arrythmias, meningitis and unilateral facial paralysis (Bell’s palsy).

Trans-stadium transmission of the bacteria occurs in Ixodes species. The bacteria are ingested in a blood meal of the nymph from a reservoir host and with the next blood meal they enter the haemolymph of the tick and migrate to other tissues, including the salivary glands, where they can then infect other animals. Small mammals and wild birds act as reservoir hosts i.e. in the USA the reservoir host is the white-footed mouse.  Domestic animals can carry infected ticks into areas where humans live, but whether pet owners are more likely than others to get Lyme disease is not known.

The exact nature of the virulence factors of Borrelia is unknown, however, a plasmid-borne factor, possibly the one coding for surface lipoproteins, is essential for infectivity of this bacterium. Disease is as a result of inflammation. Borrelia has the ability to change its wall antigens thus avoiding immune-mediated destruction. Early disease is difficult to diagnose, in chronic disease serology can be used, but cross reaction with other tick-borne diseases is common.

The bacteria can be grown from skin biopsies, urine and blood plasma. Borrelia specific DNA sequences can be detected by qPCR in CSF, synovial tissue or fluid, blood and skin. Serum for serology.

Tetracyclines and ceftriaxone (cephalosporin) are used to treat this disease. Preventative acaricides and the removal of ticks preferably within 48 hours of attachment. A recombinant vaccine is available for humans at risk.

Avian spirochaetosis

Borrelia anserina is the cause of avian borreliosis or tick fever, a septicaemic disease of birds that is transmitted by the fowl tick, Argas persicus (soft tick) or other Argas species. In ticks the bacteria are spread transovarially and transstadially. After an incubation period of 3 to 12 days, infected birds develop a fever, exhibit a green diarrhoea, become have either purple (cyanotic) or white wattles (anaemia) and move show signs of paralysis (hanging wings). The spleen appears enlarged and mottled on post-mortem examination. Spiral bacteria are observed in Giemsa-stained blood smears. Penicillins or tetracyclines can be used to treat sick birds. The ticks nests in wood only feeding off the birds at night – treatment of wooden houses and perches with sump oil or creosote prevents nesting of the ticks.

Haemotropic mycoplasmas

Haemotropic mycoplasmas are small (0.3 – 0.8 μm), epi-erythrocytic, gram-negative bacteria that infect a wide variety of mammalian species. They formerly belonged to the genera Haemobartonella and Eperythrozoon, are vector-borne and in most animals infections are subclinical. However, they can cause fever, anaemia and icterus in some animals, especially those that are immune-compromised.

A list of the agents and the disease they cause is in the Table below.

Diagnosis of the infection is based upon blood film examination and a qPCR to detect DNA specific to the haemotropic mycoplasmas. Since animals can be sub-clinical carriers of the haemotropic mycoplasmas all blood donors should be tested for them.

The treatment of choice is a minimum of two week course of doxycycline. Treatment will reduce the clinical signs, but not always eliminate the bacteria.

Common haemotropic mycoplasmas, their hosts, their vectors (if known), and the diseases they cause

Host species	Cause	Disease distribution	Transmission/Vector
Cattle	M. wenyonii M. haemobos	Worldwide	In utero, needles, lice, biting flies
Sheep, goats and deer	M. ovis	Worldwide	Ticks, mosquitoes, lice
Llamas and alpacas	M. haemolamae	South America and Europe; Australia?	In utero
Pigs	M. suis	Worldwide	In utero, needles, Stomoxys calcitrans, Aedes aegypti, hog louse
Cats (feline infectious anaemia)	M. haemofelis	Worldwide	Fleas? biting? In utero
Dogs	M. haemocanis M. haematoparvum	Worldwide	Brown dog tick

Attachment to the erythrocytes leads to pore formation in the cell as well as immune complex deposition (autoimmune haemolytic anaemia) resulting in erythrocyte haemolysis. Hypoglycaemia can occur during the acute phase of the disease.

END OF CHAPTER