Human tick-borne disease (TBD) is an increasing health burden on the Australian community requiring wider diagnostic recognition. TBD comprises multiple specific zoonoses, some of which are well recognized and documented, including tick paralysis and rickettsial disease as reported at a Sydney University Website (Entomology).1
The present study addresses recent evidence for emerging Borrelia, Babesia, Bartonella, Anaplasma
, and Ehrlichia
infections in Australia. The study confirms previously published work on the existence of human Borrelia
infection in Australia.2
There are no further publications on human Lyme disease (LD) in the interval using a search on PubMed on October 3, 2011 for the MeSH headings of humans, Borrelia, and Australia. The study also examines the incidence of tick-borne coinfections, some of which occur in patients who have never left Australia.
The country has 75 tick species1
with general acceptance of Ixodes
spp. and Ixodes holocyclus
(Ih) in particular, as the main contenders in inducing human TBD in the country.4
The entire eastern coastline is habitat to Ih and it is known to vector human disease including rickettsial infection and tick paralysis.1
The Ih tick is colloquially named paralysis tick, grass tick, shell back tick, and several other names.1
It thrives in humid conditions along the coast, mainly in flatlands, from the north of the continent just above Cooktown in Queensland to Lake Entrance in Victoria at the very south of the continent. The region has a very high proportion of Australia’s human population.
The Ih tick has a larval, nymph, and adult form all of which require a blood meal.1
Larvae typically feed upon small animal hosts whilst nymph and adult will include larger animals. Humans are incidental hosts to the latter two forms. The tick may stay attached for up to 5–6 days before detaching if not found. Many tick bites are not observed or reported.1
Probably many of the nymph type, about the size of a poppyseed, are simply scratched off particularly if attached to the scalp. In Australia a majority of bites will come to nothing more than a non-elevated erythematous macule on the skin of up to 2 cm diameter resolving completely over a few days providing the tick is removed promptly. Some lesions grow at the bite site to form a 2–3 cm papule by the second day showing a black central eschar.8
Such a presentation is the typical appearance of Queensland Tick Typhus, a rickettsial infection, at the bite sight and untreated this is followed by a “spotted rash” of widespread distribution known as rickettsial spotted fever, a febrile illness whose erythematous macules are typically 4–5 mm in diameter.6
Erythema Migrans (EM) is a local skin reaction to a tick bite caused by Borrelia burgdorferi
sensu lato (Bb s.l.) infection.9
At this stage of infection the term Early Lyme Disease is also used and this terminology includes early systemic manifestations such as meningitis or cranial nerve neuropathy. After an initial 1-cm macular erythematous lesion, at day 2–5 or even later, the lesion will commence to grow in diameter and thicken for anywhere up to 14 days if left untreated. In Australia, the lesion will often become itchy and painful and rarely there will be central induration and paling of color which gives the bull’s eye classically referred to in LD literature. This has been the author’s observation over 20 years in his current practice in Australia. A single primary lesion must reach more than 5 cm in size to be classified as an EM and then it is considered to be pathognomonic.11
When documented in a known tick area it is also considered sufficient for a clinical diagnosis of LD.
LD is a protean multisystem illness that develops 6 months to 8 years after a tick bite that carries the borrelia spirochaete.12
Nomenclature of the stages of the disease includes the use of the terminology early disseminated LD and late disseminated disease.13
In North America a principal symptom of the disease is an arthritic illness that may have severe pain and swelling, more of large joints, and can be associated with marked general fatigue and other somatic features.13
The US Centers for Disease Control and Prevention (CDC) website further states that in the musculoskeletal system, LD produces recurrent attacks of arthritis with objective joint swelling in one or a few joints, sometimes followed by chronic arthritis.13
LD in North America may also be principally a neurological disease which is generally accepted to be the case throughout Europe and Asia. In the case load presented here it is entirely a neurological disease with symptoms of meningism, cranial neuropathy, and sometimes encephalopathy. Of importance is the large number of cranial nerves involved including sensory. Such a factor precludes diagnoses of multiple sclerosis, motor neuron disease, amyotrophic lateral sclerosis, chronic fatigue, fibromyalgia, and several others in the author’s opinion, leaving only sarcoid, bartonellosis, borreliosis, and the autoimmune neurological diseases (one of which is commonly known to every medical graduate as Guillain–Barré syndrome) as differential diagnoses. The latter residual differential diagnosis is put forward by the author after discussion with neurological colleagues.
Treatment of EM and early localized disease is usually very effective. Treatment of the later disseminated stage of the disease will usually be straight forward when identified early. Other cases can be protracted and treatment much more difficult. In this latter group there can be immune suppression known to be an innate response to the Lyme bacterium. Stricker and Winger first identified immune dysfunction demonstrated by lowered CD57 natural killer cell counts associated with LD.14
spp. are piroplasms that invade red blood cells.15
In the developing world babesiosis is frequently mistaken for malaria which it symptomatically mimics in the acute phase. Most healthy individuals recover completely from infection with this piroplasm over 4 or more weeks. A very few go on to chronic infection. The disease can be fatal in the acute stage with multiorgan failure due to intravascular hemolysis and stasis, particularly in splenectomised individuals. There is a large emerging incidence of low-grade babesiosis in association with LD in North America. Treatment for babesiosis in the presence of Lyme borreliosis is very difficult. Drug therapy is similar to that for malaria. Clinical symptoms and signs as a TBD are intermingled with those of LD, are complex, and beyond the scope of this work.
is a Gram-negative intracellular bacterium.16
Alone it has been known to be the cause of cat scratch fever particularly in pediatric medicine where it is defined by its hallmark of pink striae that are quite unmistakable. The infection causes an acute febrile illness in solitary infection. However it can also be tick-borne, and whilst attention is given to EM and LD, it can be overlooked, just as Babesia
is in the acute phase. Bartonellosis may go on to cause chronic symptoms identical to or confounding those of neuroborreliosis. Also it is extremely important in all documented cases to consider thorough cardiac assessment for both endocardial and myocardial damage. CDC gives a good overview.17
Human granulocytic ehrlichosis (HGE) alternatively known as human granulocytic anaplasmosis is an infection of the neutrophil line of white blood cells.16
The agent is a rickettsia. Onset of symptoms can be as bland as a febrile illness after exposure by typically 4 weeks. HGE can present much more seriously and can be fatal. The only significant routine laboratory finding is a low white blood cell count. The infection will only be confirmed by suspicion and further serological testing. Treatment should commence whilst waiting for serology.
Human monocytic ehrlichosis (HME) like HGE, is an infection caused by a rickettsial spp. but of the monocyte rather than of the neutrophil cell line.18
Though reported in North America, HME was not found in this study.