ANTARTICA: No Vector-Borne Disease, See Worldwide

AFRICA: Fleas - Epidemic Typhus, Plague, Tungiasis; Flies (non- mosquito) - African Trypanosomiasis, Leishmaniasis, Loaiasis, Myiasis flies, Onchocerciasis, Phlebotomus Fevers;Mosquitoes - Chikungunya virus, Dengue, Lymphatic Filariasis, Malaria, Rift Valley Fever, Sindbis, O'Nyong-nyong virus, Yellow Fever; Ticks - Boutonneuse Fever, Crimean-Congo Haemorrhagic Fever. Also see "Worldwide". ANTARTICA: no vector-borne disease, see "Worldwide". AUSTRALIA: Mosquitoes - Barmah Forest virus, Dengue, Kunjin encephalitis, Murray Valley encephalitis, Ross River virus, Sindbis; Mites - Scrub Typhus; Ticks - Queensland Tick Typhus & Flinders Island Spotted Fever, Tick Paralysis. Also see "Worldwide". CENTRAL AMERICA: Fleas - Epidemic Typhus, Tungiasis; Flies (non- mosquito) - Leishmaniasis, Onchocerciasis, Phlebotomus Fevers; Hemiptera - Chagas' Disease; Mosquitoes -Dengue, Lymphatic Filariasis, Malaria, Mayaro virus, Oropouche Fever, Venezuelan Equine Encephalitis, Western Equine Encephalitis, Yellow Fever; Ticks - Rocky Mountain Spotted Fever, Tickborne Relapsing Fever. Also see "Worldwide". EUROPE: Flies (non-mosquito) - Leishmaniasis, Phlebotomus Fevers; Mosquitoes - Sindbis, Ockelbo, West Nile Fever; Ticks - Boutonneuse Fever, Crimean-Congo Haemorrhagic Fever, Lyme disease, Tickborne Encephalitis, Tickborne Relapsing Fever, Tularaemia. Also see "Worldwide". GREENLAND & associated islands, ICELAND: see "Worldwide". INDIA, MIDDLE EAST (and other subcontinent nations): Fleas - Epidemic Typhus, Murine Typhus, Plague; Flies (non- mosquito) - Leishmaniasis, Phlebotomus Fevers; Mites -Scrub Typhus; Mosquitoes - Chikungunya virus, Dengue, Japanese Encephalitis virus, Lymphatic Filariasis, Malaria, Powassan Encephalitis, Sindbis, West Nile Fever; Ticks -Boutonneuse Fever, Crimean-Congo Haemorrhagic Fever, Kyasanur Forest Disease, Tularaemia, Tickborne Relapsing Fever. Also see "Worldwide". NEW GUINEA & western Pacific Islands: Mites - Scrub Typhus; Mosquitoes - Dengue, Japanese Encephalitis virus, Lymphatic Filariasis, Malaria, Murray Valley Encephalitis. Also see "Worldwide". NEW ZEALAND: no vector-borne disease but Simulid flies (locally called sandflies) can be of serious nuisance biting in the south Island, also see "Worldwide". NORTH AMERICA: Flies (non-mosquito) - Phlebotomus Fevers; Fleas - Epidemic Typhus, Murine Typhus, Plague; Mosquitoes - Dengue, Eastern Equine Encephalitis, Powassan Encephalitis, St Louis Encephalitis, Western Equine Encephalitis; Ticks - Colorado Tick Fever, Human Babesiosis (US only), Human Ehrlichiosis, Lyme disease, Rocky Mountain Spotted Fever, Tickborne Relapsing Fever, Tick Paralysis, Tularaemia. Also see "Worldwide". RUSSIA (includes former USSR countries): Mosquitoes - Powassan Encephalitis, Sindbis, West Nile Fever; Fleas - Plague; Flies (non- mosquito) - Phlebotomus Fevers; Mites -Scrub Typhus; Ticks - Crimean- Congo Haemorrhagic Fever, Issyk-Kul Fever, Lyme disease, Omsk Haemorrhagic Fever, Siberian Tick Typhus, Tickborne Encephalitis, Tickborne Relapsing Fever, Tularaemia. Also see "Worldwide". SE ASIA, CHINA & JAPAN: Fleas - Epidemic Typhus, Murine Typhus, Plague; Mites - Scrub Typhus; Mosquitoes - Chikungunya virus, Dengue, Japanese Encephalitis virus,Lymphatic Filariasis, Malaria, Powassan Encephalitis, Sindbis; Ticks - Crimean-Congo Haemorrhagic Fever, Lyme Disease (China & Japan),Tularaemia. Also see "Worldwide". SOUTH AMERICA: Flies (non- mosquito) - Bartonellosis, Leishmaniasis, Myiasis flies, Onchocerciasis, Phlebotomus Fevers; Hemiptera - Chagas' Disease; Fleas - Plague; Tungiasis;Mosquitoes - Dengue, Lymphatic Filariasis, Malaria, Mayaro virus, Rocio Encephalitis, Venezuelan Equine Encephalitis, Western Equine Encephalitis, Yellow Fever; Ticks - Rocky Mountain Spotted Fever, Tickborne Relapsing Fever. Also see "Worldwide". WORLDWIDE: in all continents there are the following insect pests; Bed bugs, Bird mites, Body lice, Dust mites, Head lice, Pubic lice and Scabies. Plus there are various members from the following groups, although the species will vary from country to country; Ants, Bees, Cockroaches, Fleas, Flies (both biting and non-biting), Mosquitoes, Scorpions, Spiders, Ticks,Urticating Caterpillars and Wasps.

Bed bugs

 Introduction  Natural History  Clinical Presentation  Laboratory Diagnosis  Treatment and Control  Confirmation and Enquiries modified from: Service, M.W. (1980). A guide to Medical Entomology. Macmillan. London.

bottom of page News! We now have a dedicated Bed Bug web site: www.bedbug.org.au This site contains much more detail on bed bug control and includes numerous research papers.

Introduction Bed bugs were once a common public health pest worldwide, which declined in incidence through the mid 20th century. Recently however, bed bugs have undergone a dramatic resurgence and worldwide there are reports of increasing numbers of infestations. Australia has also been included in this trend and the Department of Medical Entomology, ICPMR, has been at the forefront of documenting this phenomena and providing information on the ecology and control of this important public health pest.

Natural History Bed bugs are wingless insects, roughly oval in shape, 4-5mm long when fully grown, and are fast runners. They are rust brown in colour and change to a deeper red brown following a blood meal. Bed bugs are dorsoventrally flattened and being thin means that they can hide in narrow cracks and crevices, making detection often very difficult. The two main species that bite humans include the common bed bug, Cimex lectularius, and the tropical bed bug, Cimex hemipterus. The presence of the former species has been long known in Australia, whereas the tropical bed bug was only recently recognised in the country by the Medical Entomology Department, ICPMR. There are five juvenile stages known as nymphs, which are miniature versions of the adults in appearance. Each nymphal stage requires at least one blood meal to moult to the next stage and it takes 5-10 minutes for complete engorgement to occur. The entire nymphal development takes 6-8 weeks, while the adult bed bugs can live on average for 6-12 months. All nymphal stages and adults of both sexes require blood for nutrition and development. After mating, each female lays 2-3 eggs a day throughout her lifespan. The cream coloured eggs (1mm in length) are cemented on rough surfaces of hiding places, and will hatch within around 10 days at room temperature, but longer in cooler conditions. The mouthparts of bed bugs are especially adapted for piercing skin and sucking blood. Like most blood sucking arthropods, they inject saliva during feeding, which has anticoagulant properties. Bed bugs respond to the warmth and carbon dioxide of a host and quickly locate a suitable feeding site. They tend not to live on humans and the only contact is for a blood meal. Most blood feeding occurs at night, and they generally seek shelter during the day and become inactive while digesting the blood meal. However, bed bugs are opportunistic and will bite in the day especially if starved for some time. They can survive for long periods without feeding. While their preferred host is human, they will feed on wide variety of other warm-blooded animals including rodents, rabbits, bats, and even birds. Being a cryptic species, bed bugs shelter in a variety of dark locations, mostly close to where people sleep. These include under mattresses, floorboards, paintings and carpets, behind skirting, in various cracks and crevices of walls, within bed frames and other furniture, and behind loose wallpaper. Bed bugs tend to stay in close contact with each other and heavy infestations are accompanied by a distinctive sweet sickly smell. Blood spotting on mattresses and nearby furnishings is often a tell tale sign of an infestation. Bed bugs are one of the great travellers of the world and are readily transported via luggage, clothing, bedding and furniture. As such, they have a worldwide distribution.

Clinical Presentation Skin reactions are commonly associated with bed bugs, which result from the saliva injected during feeding. Some individuals however, do not react to their bite, whereas others note a great deal of discomfort often with loss of sleep from the persistent biting. The most commonly affected areas of the body are the arms and shoulders. Reactions to the bites may be delayed; up to 9 days before lesions appear. Common allergic reactions include the development of large wheals, often >1cm, which are accompanied by itching and inflammation. The wheals usually subside to red spots but can last for several days. Bullous eruptions have been reported in association with multiple bed bug bites and anaphylaxis may occur in patients with severe allergies. In India, iron deficiency in infants has been associated with severe infestations. It has been suggested that allergens from bed bugs may be associated with asthmatic reactions. Bed bugs have been implicated in the transmission of a wide variety of infectious agents, although their status as vectors is uncertain. It has been suggested that they might play a role in the spread of hepatitis B, however, experimental evidence does not support this. Note that an irritation or bite experienced in bed may not necessarily be due to a bed bug infestation.

Laboratory Diagnosis A bed bug infestation can be diagnosed by the identification of specimens collected from the infected residence. Collection of live or dead bed bugs, cast skins, hatched or unhatched eggs will determine an infestation. There are two species of bed bug that bloodfeed on humans but Cimex lectularius has the most widespread international distribution; the other species, C. hemipterus, is usually confined to tropical regions.

Treatment and Control If bed bugs are suspected then a licensed pest controller should be consulted. A careful inspection must be undertaken and all possible hiding places within infested and adjoining rooms examined. Once all likely sources have been identified, then an approved insecticide, which has some residual activity, should be applied to all harbourages. The synthetic pyrethroids are often the main chemicals used for control in Australia, however these are not very effective and can even repel the bugs. The carbamates and the organophosphates are far more effective for control, but may not be recommended for use on mattresses (check the label). Non-chemical approaches to control include the use of vacuuming and steam. Infested clothing can be washed in hot water and dried on the hot cycle of the clothes drier. Delicate materials can be placed into the freezer. Pesticides will need to be applied in conjunction with any non-chemical means of control. Good housekeeping practices and a reduction in possible harbourages such as cracks and crevices will discourage repeat infestations. As bed bugs are cryptic in their habits, complete control is often difficult to achieve with the first treatment. This is especially so with heavy infestations and thus a post control treatment evaluation is always advisable. For more information on control visit our Bed Bug web site & click on the Bed Bug Code of Practice (or click here).

Confirmation and Enquiries Identification of bed bugs, and other medically important insects, is performed through the Medical Entomology Department at ICPMR, Westmead Hospital. The Medical Entomology Department is the only NATA accredited laboratory in Australia for the identification of arthropods of medical importance. Bird Mites

 Introduction  Natural History  Clinical Presentation  Laboratory Diagnosis  Treatment and Control  Confirmation and Enquiries

Bird Mite (Ornithonyssus bursa)

bottom of page Introduction Bird mites belong to a group of arthropods, which are morphologically very similar in appearance, yet have very different habits and ecologies. Failure to properly identify the mites to the species level can lead to incorrect treatments and non-control of the pest. Mites should be referred to an expert laboratory for proper identification, such as the Department of Medical Entomology, ICPMR.

Natural History

"Bird mites", "Tropical fowl mites" or "Starling Mites" are the common names used to describe the mite Ornithonyssus bursa from the family of mites Macronyssidae. These mites are often incorrectly called 'bird lice', particularly within the pest control industry. Bird mites are most active during Spring and early Summer. Ornithonyssus bursa is a small but extremely mobile mite, barely visible to the eye, with eight legs (except the larva that has 6), oval in shape and with a sparse covering of short hairs. The mite is widely distributed throughout warmer regions of the world. It is a parasite, feeding on the blood of common birds including pigeons, starlings, sparrows, Indian mynahs, poultry, and some wild birds. Bird mites are semi-transparent in colour, which makes them difficult to detect on skin until blood is ingested and then digested; when they may appear reddish to blackish. Contact with humans usually occurs after birds gain entry to roof cavities via broken tiles or through unprotected eaves, of homes, factories, barns and other dwellings to construct their nests in early spring or summer. However, some infestations also occur from birds roosting on the outside of dwellings such as window ledges or awnings. The mites feed on the unfeathered nestlings, as well as the adult birds, and the large amount of nesting material used by the birds provide the mites with an ideal environment in which to thrive. The mites have a short life cycle (approximately 7 days) and can rapidly generate large populations. When the young birds leave the nest, or die, many mites (often many tens of thousands) are left behind in the absence of a suitable host, and these will disperse from the nest into and throughout the dwelling searching for new hosts. Most mites will die within 3 weeks without a blood meal from a bird host. They will bite humans they encounter but cannot survive on humans.

Clinical Presentation As a result of their 'test biting' while searching for a new bird host, the mites inject saliva. This can lead to severe irritation with rashes and intense itching. Scratching of the bites may result in secondary infections. Bird mites are not associated with the transmission of any infectious disease. The bites are often difficult to diagnose and can be mistaken for bites from a number of other arthropods. The greatest impacts from bird mites are usually experienced in rooms close to the point of entry of the mites. The mites have no preference for any particular areas of the body and they do not live underneath the skin, nor can an infestation be maintained on humans. However, the problem will persist while the bird-related source of the mites remains. Until the infestation is controlled, the occupants of the building can experience considerable discomfort. Also, the sensation of crawling mites on the skin will irritate some people.

Laboratory Diagnosis Identification by high-power light microscopy, using appropriate taxonomic keys, by an expert is the only method of correctly identifying the mite. Although Ornithonyssus bursa is the most common mite associated with infestation of homes there are several other mites associated with birds within Australia that can invade dwellings and bite humans. These bird mites includeOrnithonyssus sylviarum (Northern fowl mite) and Dermanyssus gallinae (Chicken mite). Also, a closely related species, Ornithonyssus bacoti (Tropical rat mite), occasionally attacks humans. This species is associated with rodents, such as rats and mice, and their nests. Ornithonyssus bursa and Ornithonyssus bacoti are taxonomically very similar and are extremely difficult to differentiate. Correct identification is absolutely necessary if appropriate control procedures are to be recommended.

Treatment and Control The irritation associated with bites can be alleviated with an anti-pruritic such as crotamiton (e.g. EURAX®) but there is no specific treatment. Severe reactions may have to be treated as for other allergic conditions with antihistamines. Unless steps are taken to control the mite infestation, symptoms resulting from bird mite bite will continue. Once the mite has been correctly identified, appropriate steps must be taken to locate and remove the source/s of the infestation and prevent its recurrence. All nesting sites should be located and nesting material removed. An insecticidal spray can be applied to ensure total eradication of mites, but treatment of rooms without removal of nests in roof cavities will not stop further mites entering and the problem will continue. Broken tiles or timber allowing access to roof cavities should be repaired and all potential entry points to the eaves and roof cavity blocked. Roosting and nesting sites on window ledges should be cleared and made unsuitable for future bird use. A pest control officer may have to be employed to undertake these control measures, especially if large areas are involved. Biting Flies

 Natural History  Clinical Presentation  Laboratory Diagnosis  Treatment and Control  Confirmation and Enquiries

modified from: Kettle, D.S. (1995). Medical and Veterinary Entomology. CAB International. Wallingford

bottom of page Natural History Biting flies are distributed throughout the world and, apart from nuisance biting, some are responsible for the transmission of diseases in humans and livestock in many countries. Although Australian biting flies (other than the mosquitoes) do not transmit diseases to humans they are renowned for painful bites and annoying habits during the summer months in general. Within Australia, the biting flies of greatest significance are the horse flies or March flies (Family Tabanidae), the stable flies (Family Muscidae) and the black flies (Family Simuliidae), as well as the biting midges or sand flies (Family Ceratopogonidae) and the mosquitoes (Family Culicidae), which are dealt with elsewhere (see Biting Midges fact sheet and Mosquito fact sheet). Compared with some other countries, black flies are usually not a concern in Australia although occasional problems occur following floods in northwestern NSW and Queensland. March flies and stable flies are widespread throughout the warmer parts of Australia and will attack humans, livestock and domestic pets to acquire blood. The flies are stoutly built and are strong swift fliers that tend to be more active throughout the summer months especially in still, open sunny areas. The Tabanids, especially, are influenced by weather and will respond to changes in barometric pressure, wind, cloud cover and temperature. The stable fly, Stomoxys calcitrans is a vicious biter with piercing and sucking mouthparts that can easily penetrate socks and stockings. Both sexes of this fly will search for blood meals, often twice a day, and can engorge on blood up to three times their own body weight. In the cooler months their life span is 1-2 months, in warmer weather it is reduced to 3-4 weeks of adult life. These flies are seldom found in urban situations (except where horse stables or major composting areas are nearby) and are more often associated with rural properties and domestic animals; they are also common on some beaches where they breed in sea-weed. They have been known to enter homes and other buildings to blood feed during daylight hours. March flies (Tabanids) have two large prominent eyes and are much larger and robust than stable flies; they have a shorter life than stable flies and an adult lives only 3-4 weeks. Although they are a major pest of livestock, several species will bite people. It is only the females that seek blood meals; the males feed on nectar and plant juices. Female tabanids are armed with two large blade-like mouthparts, that are used to pierce and slash skin. This inflicts a painful wound and produces a large puncture site that will continue to ooze blood long after the mouthparts are extracted. As the blood flows, the flies lap the blood to engorgement, unless disturbed. It has been estimated that some animals can loose up to 300ml of blood a day due to attack by these flies, resulting in serious blood loss. Adult tabanids are cosmopolitan but are more abundant in moist forests and woodlands. After mating, the females disperse, travelling many kilometres in search of blood meals. Tabanids are pests throughout summer and are a continual nuisance at outdoor activities, particularly near water.

Clinical Presentation Biting flies can produce an array of symptoms including pain, itching, urticaria and cellulitis. An allergic response is the most common, which imay be characterised by hives, and in some cases wheezing. Tabanid bites are very painful, with some individuals developing severe lesions, fever and general disability. This allergic response is due to the large amounts of saliva injected by the fly to prevent their blood meal from clotting. Stable flies bites are quite painful and they produce small papules that quickly fade, but are often itchy. Local symptoms can be relieved with an application of antiseptic lotion or cream and in some cases a mild oral antihistamine is prescribed. Prolonged scratching of bites may lead to secondary infections. Hypersensitivity to biting flies is rarely seen in human population.

Laboratory Diagnosis Biting flies are identified with the aid of a stereo microscope and taxonomic keys.

Treatment and Control Elimination of potential breeding sites will help in reducing fly numbers, Stable flies are attracted to decomposing organic waste, such as piles of grass clippings and compost heaps. Properly maintained compost heaps that are turned regularly will deter flies from ovipositing and thus discourage breeding. The use of repellents that contain DEET will generally deter most biting flies.

Confirmation and Enquiries Identification of biting flies, and other medically important insects, is performed through the Medical Entomology Department at ICPMR, Westmead Hospital.

Biting Flies  Natural History  Clinical Presentation  Laboratory Diagnosis  Treatment and Control  Confirmation and Enquiries

modified from: Kettle, D.S. (1995). Medical and Veterinary Entomology. CAB International. Wallingford

Laboratory Diagnosis Biting flies are identified with the aid of a stereo microscope and taxonomic keys.

Confirmation and Enquiries Identification of biting flies, and other medically important insects, is performed through the Medical Entomology Department at ICPMR, Westmead Hospital.

Biting Midges (Sandflies)  Natural History  Clinical Presentation  Laboratory Diagnosis  Treatment and Control  Confirmation and Enquiries

modified from: Kettle, D.S. (1995). Medical and Veterinary Entomology. CAB International. Wallingford

bottom of page Natural History Biting midges are small robust insects with piercing and sucking mouthparts that belong to the family of flies Ceratopogonidae. Only a few groups within this family are known to suck blood and their distribution is almost world wide. These small flies are renowned for their nuisance biting associated with habitats such as coastal lagoons, estuaries, mangrove swamps and tidal flats. In Australia these flies are commonly known as sandflies but are correctly referred to as biting midges. The biting activity of adult biting midges is mainly limited to the periods of dawn and dusk; they will remain inactive through very windy weather, finding shelter amongst vegetation. Biting midges will usually disperse only short distances from their breeding sites. Only female midges feed on blood, but both the females and males will feed on vegetable fluids and nectar. Adults midges are 1.5-4.0 mm long with stout short legs, and at rest fold their wings, which are often mottled, over the abdomen. Their mouthparts are short and projected down. Female midges may attack humans in large numbers, biting on any areas of exposed skin, and often on the face, scalp and hands. Some species will blood feed on a wide range of animal hosts. The egg batches contain between 30-100 eggs, and are laid on selected substrates such as mud, decaying leaf litter, damp soil or other vegetative materials, dependent on the species. The small eel-like larvae hatch in a few days; their larval habitat must contain a proportion of organic material with a high moisture content to provide optimum conditions for the larval stage to thrive and pupate. The whole life cycle takes 3-10 weeks, dependent on species and environmental conditions, particularly temperature.

Clinical Presentation Biting midges are responsible for acute discomfort, irritation and severe local reactions. Itching may commence immediately after the bite, but often not for some hours later, and most individuals are unaware of being bitten at the time. Biting midges have their greatest impact on people arriving to an area or tourists. Local residents seem to build up some immunity to the biting. In some sensitive people, midges can produce persistent reactions that blister and weep serum from the site of each bite and these reactions may last for several days to weeks. Biting midges are not known to transmit any disease-causing pathogens to humans in Australia.

Laboratory Diagnosis Identification of biting midges is performed with the use of light microscopy and taxonomic keys, after the specimen has been especially prepared on a glass slide.

Treatment and Control There are no known efficient methods of controlling biting midges, but personal protection will help in reducing exposure to their bites. Avoid localities, especially at dawn and dusk, that are known to be frequented by biting midges; wear protective clothing (long sleeves/pants), and apply a repellent to exposed skin. These measures will assist in limiting exposure to these biting flies. Irritation associated with bites may be alleviated with anti- pruritic preparations such as EURAX�, but severe reactions may require medical treatment with antihistamines.

Confirmation and Enquiries Information and identification of biting midges, and all other medically important insects, is provided through the Medical Entomology Department at ICPMR, Westmead Hospital.

Body Lice

 Natural History  Clinical Presentation  Laboratory Diagnosis  Treatment and Control  Confirmation and Enquiries

modified from: Service, M.W. (1980). A guide to Medical Entomology. Macmillan. London.

bottom of page Natural History Pediculus humanus, or the body/clothing louse is a blood sucking species of louse that can live between the skin and clothing of humans. This host specific ectoparasite of humans is thought to have evolved from head lice (Pediculus capitis) but migrated to the body in association with the wearing of clothes. Body lice are small flattened insects with a slightly elongated lobed abdomen, a distinct head, small eyes, a pair of short antennae and six legs, each terminating in a strong claw. Each of these stout claws has a small thumb-like spine for grasping, enabling the louse to move quickly around the clothes utilising the fibres of the fabric or body hair for support. Adult lice are 2-4mm in length, grey in colour, but redden after blood feeding. The mouth parts are tube-like, armed with minute teeth and sharp stylets for piercing the skin, and when not in use, are telescoped within the head. Adult lice and the three nymphal (immature) stages live their entire life within the clothing of humans. Lice may only leave the clothes briefly or hold onto the fibres of clothes or body hair whilst blood feeding. The lice blood feed frequently, at any time, day or night, but usually when the person is at rest. These parasites prefer to feed where the skin is soft and folded and the clothing fabric is in close contact with the body. Female body lice will lay their eggs (or nits) along the seams or hems of clothes (especially underwear) that are adjacent to the surface of the skin. Each egg is firmly glued to fibres of the clothes, but occasionally body hair maybe used. A mature female louse will lay 200-300 eggs within her life span of a month, laying between 6-9 eggs a day. The eggs are white and oval in shape and rounded at the top. Eggs hatch within 5-10 days, but if the clothing is removed each night from the warmth of the body, development time is increased and the eggs may take up to 2 weeks before hatching. Louse eggs can remain viable for up to 14 days. Body lice are extremely sensitive to change in temperature and humidity and have been known to abandon a dead person or people with elevated temperatures. Without a constant source of blood, the lice perish within 2-5 days. In hot weather, when several layers of infested clothing are worn, the lice may move to an outer layer where the temperature is cooler. Lice are very rarely seen crawling on the outside of infested clothes, if they are visible it is an indication the individual is heavily infested. Normally body lice are sensitive to light and if disturbed will quickly move to a seam or crease for cover. Transmission of body lice occurs when living conditions are crowded, personal hygiene is neglected, clothes are not changed and facilities for laundering clothes are not available. Lice can spread rapidly through homeless people or victims of war and natural disasters, when people sleep in their clothes and huddle together for warmth. Bedding and furniture have also been implicated as a source of infestation in overcrowded environments. Clinical Presentation Initially, bites from body lice are seen as small minute red dots that develop into papular lesions with wheal-like inflammation. The toxic effects from repeated injections of saliva may produce symptoms including headache, lassitude, loss of appetite, joint pain, elevated temperature, irritability, and a rash which is similar to German measles. Severe itching is another symptom that infected individuals suffer, which may indicate the development of an allergy; inhalation of faeces or parts of cast skins from body lice may also trigger symptoms which resemble hay fever. Secondary infections are common and result from the continuous scratching of repeated inoculations of louse saliva. A prolonged infestation of body lice can result in thickening and pigmentation of the skin and is often referred to as "vagabonds’s disease". Body lice are not responsible for the spread of any infectious disease-causing organisms within Australia, and are considered uncommon in this country.

Laboratory Diagnosis Identification of louse specimens is by light microscopy. Detail from the patient on exactly what part of the body the specimens were collected is important in establishing the identity of the louse. Head lice, Pediculus capitis (see Head Lice), are taxonomically very difficult to differentiate from body lice. Body lice are rarely found on the head of an infected person and, when not on the body, tend to stay hidden within layers of clothes. Pubic lice, Pthirus pubis, (see Pubic Lice), are usually found attached to the hair in the pubic and perianal areas of the body, but are taxonomically very different to the body and head louse, and are readily identified.

Treatment & Control Body lice are relatively easy to control by implementing a few simple steps. Regular changing and laundering of clothes (especially underwear), or disposal of affected clothing, will control lice. Using a hot water wash on clothes, followed by ironing will ensure all lice and nits have been killed. An increased level of personal hygiene with regular bathing or showering is essential for control. Dry cleaning or tumble drying affected items at >60oC for 15 minutes is another method of effectively killing lice and eggs. If laundering facilities are not available dusting clothes with an insecticidal powder or fumigant are options that could be considered to aid in the control of lice; as a last resort, storage of clothes in a plastic bag should see all lice and eggs dead after a month.

Caterpillars  Natural History  Clinical Presentation  Laboratory Diagnosis  Treatment and Control  Confirmation and Enquiries modified from: CSIRO. (1991). Insects of Australia. 2nd ed. Melbourne University Press, Victoria.

bottom of page Natural History Australian Lepidoptera (moths and butterflies) contain several species of caterpillars that are armed with stinging hairs and/or fragile spines. These modified hairs serve as an effective means of protection against predators intertested in the soft bodied caterpillars. Skin contact with these specially equipped caterpillars can produce severe irritation and inflammation which is often referred to as lepidopterism. The body surface of various urticating (irritating) caterpillars are adorned with microscopic dart hairs, or rigid bristles, or long and flexible tapering hairs. Hairs may be arranged in a pattern or tubercle on the side or dorsal surface of the caterpillar, depending on the species. The location and structure of the hairs, or group of hairs on the insect, can be used as a diagnostic tool to identify the species of caterpillar. Urticating hairs can be of two distinct types. The first are envenomating hairs, which are tubular or porous spines capable of holding a venom or irritant produced by a gland at the base. On contact, the tips of the hair break under pressure and release their fluid contents, which is generally a mixture of histamines. There are only two families of lepidoptera within Australia that have caterpillars which possess these stinging hairs; they are the Limacodidae ("cup moths" or "Chinese junk" caterpillars) and the Nolidae (gumleaf skeletonisers). Other hair types on caterpillars are referred to as non- envenomating hairs and these produce a mechanical irritation on contact. These hairs are fragile and easily dislodged from the caterpillar, they adhere to the surface of skin when the caterpiller is contacted, or they become airborne and on settling the barbed or dart hairs easily fragment and penetrate clothing or skin. Hairs that are air-borne can drift and settle on nearby washing or other surfaces whichhumans will contact. Accidental disturbance or handling of old larval skins and spent cocoons, deposited under leaf litter, bark, wood piles, timber or any other material that caterpillars have had contact with, can result in irritation. These hairs retain their urticating properties long after the caterpillars have pupated. The families of Lepidoptera that contain these special hairs include, the Arctiidae (tiger moths), Anthelidae (white stemmed gum moth), Eupterotidae (bag shelter moths), Lymantriidae, the tussock moths (mistletoe brown-tail moth and the white cedar moth) and Notodontidae (bag shelter moth and processionary caterpillars).

Clinical Presentation The intensity of the irritation, whether it be caused by "venomous" or "irritating" hairs, will be dependent on the species of caterpillar and the sensitivity of the patient. Patients that come in contact with urticating hairs usually develop wheals and widespread rashes which can be accompanied by a burning sensation. Other symptoms include dermatitis, papules, pain, itching and swelling of the infected area. This inflammation can persist for days, although in most cases the symptoms are transitory. If mucous membranes have been affected there may be some swelling and irritation. Detached hairs can also be inhaled and the upper respiratory tract can be affected producing dyspnoea or laboured breathing. Injuries to the eye have been recorded, resulting in conditions such as nodular conjunctivitis and, less commonly, permanent damage to the cornea. In the case of a mistletoe browntail caterpillar infestation, large numbers of school age children have been known to become affected after sitting under infested Eucalyptus trees, or as a result of disturbing leaf litter and bark at the base of the trees where the caterpillars have rested or pupated.

Laboratory Diagnosis Accurate identification is essential in treating and controlling caterpillar infestations. This should be undertaken by experienced staff, with the use of light microscopy and taxonomic keys.

Treatment and Control To treat irritations as a result of urticating caterpillars, remove all affected clothing and apply a piece of adhesive tape to each of the affected areas, then pull the tape off immediately. This will remove some of the hairs and irritants and reduce the full impact of the irritation. The use of analgesics, creams, antihistamines and lotions with steroids will also assist in relieving the symptoms. Avoid handling any hairy caterpillars or material with which they have been in contact. Suitable protective clothing, including eyewear and gloves should always be worn when handling these insects. Most caterpillar infestations are usually short lived and should be left undisturbed, unless they are causing a problem, when intervention by a reputable pest control officer would be recommended. Many infestations will die out either through predation or when all food sources are exhausted. However, some preventative control measures should remain in place to guard against Mistletoe browntail infestations especially in or near school yards. The removal of all mistletoe from Eucalypt trees within school yards or nearby areas before spring will prevent colonisation. Bare soil or mulching with pebbles at the base of existing eucalypt trunks will help deter pupation and resting of the caterpillar stage. Planting tree species that do not attract infestations, when shade is required in school yards or backyards, is another means of avoiding the problem.

Confirmation and Enquiries Identification of caterpillars and all other medically important arthropods is preformed through the Medical Entomology Department at ICPMR, Westmead Hospital.

Dengue Overview Natural History Symptoms Laboratory Diagnosis Treatment Prevention Further Reading

bottom of page Overview Currently, dengue is the most important viral disease transmitted by mosquitoes afflicting humans in a world context. Clinical symptoms range from mild fevers, to a severe and potentially life threatening haemorrhagic disease. Source reduction of the breeding habitats of the major mosquito vector, Aedes aegypti, is the best form of control.

Natural History The normal cycle of dengue infection is considered to be human - mosquito - human. From feeding on an infected and viraemic human, the female mosquito is able to transmit the dengue virus after an incubation period of 8- 10 days wherein virus infection, replication and dissemination result in infection of the salivary glands making the mosquito infective for life. In Australia epidemics of dengue occurred in the late 19th century and early 20th century. Australia was considered to be free of local dengue following 1955 (when there had been a large outbreak in Townsville), but in 1981 a major outbreak with an estimated 3,000 infections occurred in northern Queensland, presumably initiated by an infected traveller. In Australia, there are three possible vectors: Ae. aegypti, whose distribution is restricted to Queensland; Ae. scutellaris, which is present in north Queensland and is a known vector of dengue in Papua New Guinea; Ae. katherinensis, which is found in northern Queensland, the Northern Territory and northern Western Australia but appears to be not an effective vector. Additionally, Ae. albopictus, poses a threat to Australia. It is an important vector that has been introduced from Asia to many countries, as eggs or larvae transported in artificial container habitats such as used motor vehicle tyres, and water barrels on ships. If it was introduced to Australia it is likely it could readily establish and present a threat for dengue transmission. It is assumed that Ae. aegypti is the vector of greatest concern because of its distribution and close association with humans. Ae. aegypti is predominantly a day-biting mosquito whose larvae may be found almost exclusively in clean water in man-made containers such as water-barrels, rainwater tanks, wells, vases, tyres, bottles, tins, and most other water-holding containers found in the domestic environment. Although the species is currently restricted to Queensland, there are past records of Ae. aegypti being found in NSW, the NT and WA.

Symptoms Dengue is a debilitating infection of comparatively short duration with a high attack rate but a low fatality rate. The so-called 'classical' Dengue Fever (DF) form usually affects older children and adults with fever, violent headache, and severe pains in the muscles and joints following an incubation period of 5- 8 days, and lasts about 4-7 days; recovery is generally complete although convalescence may be long. A more severe form, Dengue Haemorrhagic Fever (DHF), involves internal bleeding and is sometimes associated with severe shock (the Dengue Shock Syndrome (DSS)), and occurs most frequently in infants and young children. Dengue virus occurs as four serotypes, designated DEN 1, 2, 3 and 4; each has been involved in both uncomplicated dengue and in cases with haemorrhagic syndrome.

Laboratory Diagnosis A variety of blood tests are used to demonstrate the presence of specific antibodies to Dengue virus. Blood samples should be taken during the acute and convalescent phases of the illness, and a fourfold rise in antibody levels will confirm the clinical diagnosis.

Treatment No specific antiviral treatments exists nor is there any vaccine available. For patients with DHF or DSS, treatment is supportive.

Prevention Restricting the availability of potential breeding habitats for Ae. aegypti will help to reduce mosquito densities and therefore reduce the possibility of disease transmission. All containers capable of holding water in the domestic environment can provide habitat for the larval stage of the mosquito and this includes water-barrels, rainwater tanks, wells, vases, tyres, bottles, potplants saucers and tins. Personal protective measures include: avoiding known mosquito infested areas, especially at dawn and dusk when mosquitoes are most active; ensuring that houses are adequately fly screened (with small mesh); using insect repellents that contain the chemical DEET, and reapplying it regularly; and wearing long sleeved shirts and pants.

Further Reading Boughton, C.R. (1996). Australian Arboviruses of Medical Importance. Royal Australian College of General Practitioners, Melbourne, pp 67. Gubler, D.J. (1988). Dengue. in Monath, T. (ed). The Arboviruses: Epidemiology and Ecology, Volume II. CRC Press, Florida, pg: 233-261. Gubler, D.J. and Kuno, G. (eds). (1997). Dengue and Dengue Hemorrhagic Fever. CAB International. Cambridge. Dog Heartworm

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The dog heartworm, Dirofilaria immitis, is an increasing major veterinary health problem for dogs. Although heartworm in Australia has in the past been considered to be mainly a problem of tropical and subtropical coastal regions, in recent decades it has become increasingly prevalent in more southern areas. Adult female worms in the dog's heart produce microscopic embryonic microfilariae which circulate in the peripheral blood. After ingestion, the microfilariae migrate from the mosquito's midgut, undergo development involving two moults, and after a period of approximately two weeks the infective third stage larvae migrate towards the mosquito's head. These larvae then transfer to the skin of the final host during feeding of the infected mosquito. Following their penetration into the final host, the third stage larvae migrate through body tissue where they develop into fourth stage larvae, then immature adults which finally enter the blood stream and reach the heart via the venous system. Adults mature in about 6 months and are subsequently found in the heart and major vessels. The adults mate, and the female produces millions of microfilariae to circulate in the peripheral blood to renew the cycle. The dog can be severely affected, with major vessels becoming blocked with chronic infections; death usually results in such cases from heart failure. Mosquito vectors in all parts of Australia have not been adequately identified, although in southeastern Australia, Aedes notoscriptus and Culex annulirostris are prime suspects because they have been shown to be infected in field studies and are very good laboratory vectors. The former species is an excellent laboratory vector, has close contact with dogs in domestic and peri-domestic urban, and rural situations, and is thus suspected to be a very important vector. In certain circumstances Ae. vigilax, Ae. camptorhynchus, Cx. quinquefasciatus and An. annulipes, and possibly other species may need to be considered as local vectors.

Dust Mites  Natural History  Clinical Presentation  Laboratory Diagnosis  Treatment and Control  Confirmation and Enquiries

modified from: Kettle, D.S. (1995). Medical and Veterinary Entomology. CAB International. Wallingford

bottom of page Natural History The most common species of dust mite isolated in Australia is Dermatophagoides pteronyssinus from the family Pyroglyphidae, but there are other species of dust mite as well as predatory mites that share the same dusty environment. Dust mites live in the fine layer of minute dust particles that continually settles on household items. They are found almost world wide but their numbers are considerably reduced at high altitudes and dry climates. House dust mites have been known to be associated with allergies since the 1960's and have become a focus over the years for their involvement with respiratory ailments. They do not bite or sting but harbour strong allergens in their bodies as well as in their secretions, excreta and shed skins. Constant contact with these allergens can trigger respiratory and dermatological complaints in some humans. Dust mites favour homes with high humidity levels and constant warm temperatures, and under these conditions mite populations explode, although there are some seasonal fluctuations. The mites are known to concentrate in high traffic areas in homes and on certain furniture items, especially beds, upholstered lounges, chairs, and in carpets with long fibres. They are attracted to these areas for food, and they feed on shed human skin scales and secretions, house dust, fungal spores, pollen grains, plant fibres, and insect scales. Dust mites dislike strong light and will take harbourage in the seams, ledges, and framework of furniture when exposed. Due to their light weight, dust mites can become airborne during activities such as bed making, and in this way can be distributed throughout the room or house. Adult mites are described as white to a light tan in colour; they are difficult to see with the naked eye, as they measure only 0.5mm in length, and the developmental stages are smaller. The body of the mite is oval shaped and covered with fine striations. There are five stages in the life cycle of a dust mite; from the egg, the larvae stage, then two nymphal stages, and finally the adult. The whole life cycle from egg to adult takes approximately one month to complete, mature female mites can lay from 1-2 eggs per day. Adult mites can live up to two months but this is dependent on the levels of humidity and temperature of their surrounding environment.

Clinical Presentation There is not one single clinical symptom that can readily identify mite-allergic asthmatic patients. This makes a clinical diagnosis difficult, and is therefore dependent on the reporting of other associated features. There is a proliferation of allergy clinics that specialise in testing for allergic responses to different materials including dust mites using skin prick tests. Medical conditions that are attributable to the presence of dust mites include allergic rhinitis, asthma, childhood eczema and other allergic conditions. Dust mites do not transmit any disease-causing pathogens.

Laboratory Diagnosis Identification of dust mites is performed with the use of light microscopy and taxonomic keys, after the specimen has been extracted by flotation and/or sieving methods from the dust substrate and especially prepared on a glass slide.

Treatment and Control Allergies from house dust mite can be managed by immunotherapy using mite extracts in conjunction with reducing the mite population in the home of the patient. It is virtually impossible to eliminate all dust mites from a household, but areas where mites tend to congregate can be targeted. Wall to wall carpet should be reduced, and replaced where possible with smooth hard surfaces that are easy to clean. Upholstered furniture can be avoided, mattresses and pillows should be encased in especially manufactured (‘plastic’) products that aid in the exclusion of mites. Bedding and curtains should be selected on their ability to withstand frequent laundering. Thorough vacuuming on a regular basis, including all mattresses, especially the seams and framework of the bed, will also help. A reduction in humidity levels by increased air circulation and ventilation throughout the house will assist in maintaining mites at a lower level.

Vector-Borne Diseases

Ross River disease & Barmah Forest disease (mosquitoes) Australian, Murray Valley and Kunjin encephalitis (mosquitoes)

Japanese Encephalitis (mosquitoes)

Dengue Fever (mosquitoes)

Dog Heartworm (mosquitoes)

Malaria (mosquitoes)

Lyme disease (ticks)

Spotted Fevers (ticks)

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Medically Important Arthropods

Ants, Bees & Wasps

Bed bugs

Caterpillars Entomophobia Delusionary Parasitosis ? Illusionary Parasitosis

Fleas

Flies - Biting

Flies - Biting Midges (Sand Flies)

Flies - Non biting

Flies - Mosquitoes

Flies - Myiasis

Lice - Body

Lice - Head

Lice - Pubic

Mites - Bird

Mites - Dust Mites - Scabies

Scorpions

Spiders

Ticks

Travel Bugs

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Ross River & Barmah Forest Overview Natural History Symptoms Laboratory Diagnosis Treatment Prevention Further Reading

bottom of page Overview Traditionally known as Epidemic Polyarthritis, both Ross River (RR) and Barmah Forest (BF) disease are caused by viruses which are transmitted to humans through the bite of mosquitoes. A wide variety of symptoms may occur from rashes with fevers, to arthritis that can last from months to years with RR virus infection. There are no specific treatments and actions which reduce mosquito bites are the best form of prevention against these debilitating diseases.

Natural History RR disease is the most commonly transmitted mosquito-borne viral disease to humans in Australia. The number of cases has averaged >5,000 per annum during 1991-1997. The virus appears to be endemic in most rural areas, and there has been an increasing incidence near major cities. BF disease is less common, but the number of cases appears to be increasing annually, with several outbreaks occurring during the1990's. (For annual number of cases, visit the National Notifiable Diseases Surveillance System web page: http://www.health.gov.au/pubhlth/cdi/nndss/nndss2.htm). For most of Australia, peak incidence of the diseases is through the summer and autumn months, particularly from January through to March, when the mosquito vectors are most abundant. However, in southwestern Australia and eastern Victoria, RR activity often begins in the spring months and peaks in early summer. Areas under intensive irrigation and localities close to saltmarshes, are most productive for mosquito populations and hence tend to result in the highest number of human cases of disease. Outbreaks occur when local conditions of rainfall, tides and temperature promote vector abundance. Serological studies and laboratory investigations have indicated that native mammals, most likely kangaroos and wallabies, are natural hosts for RR virus but little is known about the hosts of Barmah Forest virus. RR virus transmission from human to mosquito to human (thus occurring without the involvement of an animal) has been proposed, and there is now little doubt that such a cycle involving only humans and mosquitoes occurs during periods of intense virus activity. RR and BF viruses have been isolated from many mosquito species, indicating wide susceptibility among mosquitoes. In inland regions, the major vector is Culex annulirostris which breeds in freshwater habitats, especially in irrigated areas. Along coastal regions, saltmarsh mosquitoes represent the major threat, including Aedes vigilax and Ae. camptorhynchus in northern and southern coastal regions respectively. There is some evidence that 'floodwater' Aedes species such as Ae. normanensis play an important role in transmission in inland regions following heavy rains or floods, and Coquillettidia linealis is a secondary vector in areas with established wetlands. In the domestic urban situation, there is evidence to suggest that Ae. notoscriptus may be a vector, while Cx. quinquefasciatus is not.

Symptoms Human infection with RR virus or BF virus, may result in the clinical condition known as polyarthritis. The effects range from a symptomless condition, through a transient rash and mild illness with fever, to polyarthritis affecting chiefly the ankles, fingers, knees, and wrists, but other joints may be affected. The disease is not fatal. For RR virus, symptoms become evident from 3-21 days (average 9 days) after infection, and mild cases may recover in less than one month but many persist for months to years. Recent studies have indicated that the rash may be more florid with BF virus infections but that the arthritic symptoms are greater with RR virus infection. People of working age are most likely to be afflicted with the diseases, whilst symptoms are rare in children.

Laboratory Diagnosis A variety of blood tests are used to demonstrate the presence of specific antibodies to RR and BF virus. Blood samples should be taken during the acute and convalescent phases of the illness, and a fourfold rise in antibody levels will confirm the clinical diagnosis.

Treatment Specific therapies do not exist to treat the disease, rather it is the symptoms that are alleviated. This includes various analgesics to reduce the pain and fevers, and anti-inflammatory agents for the arthritic symptoms.

Prevention Prevention of mosquito borne viral diseases is mainly accomplished through reducing the threat of bites from mosquitoes. This can be achieved either through undertaking active mosquito control or by the use of personal protective measures. A variety of active mosquito control measures are available including habitat modification in order to reduce water availability for breeding of the larval stage, through to the use of appropriate insecticides for controlling the larval or adult stage. These are large scale control measures which can only be undertaken by government bodies, generally local councils. On a small scale, householders can ensure that their own backyard does not contain water holding containers which can provide suitable mosquito larval habitats (e.g. undrained pot plants, blocked gutters, disused bottles, old tyres, etc). Personal protective measures include: avoiding known mosquito infested areas, especially at dawn and dusk when mosquitoes are most active; ensuring that houses are adequately screened; using insect repellents that contain the chemical DEET, and reapplying it regularly; and wearing long sleeved shirts and pants. Other preventative measures include government based programs that undertake mosquito monitoring and virus surveillance from mosquitoes. These programs aim to act as an early warning system for virus activity by monitoring mosquito populations, viruses such as Ross River or Barmah Forest and weather patterns. In New South Wales, such a program has been running for several years at the Department of Medical Entomology at Westmead Hospital and is funded by the NSW Health Department.

Further Reading Boughton, C.R. (1996). Australian Arboviruses of Medical Importance. Royal Australian College of General Practitioners, Melbourne, pp 67. DOGGETT, S., RUSSELL, R., Cloonan, M., Clancy, J. and Haniotis, J. (1995). Arbovirus and mosquito activity on the south coast of New South Wales, 1994-95. Communicable Diseases Intelligence, 19: 473-475. Kay, B.H. and Aaskov, J.G. (1988). Ross River Virus Disease (Epidemic Polyarthritis). in Monath, T. (ed). The Arboviruses: Epidemiology and Ecology, Volume IV. CRC Press, Florida, pg: 93-112. RUSSELL, R.C. (1995). Arboviruses and their vectors in Australia: an update on the ecology and epidemiology of some mosquito-borne arboviruses. Review of Medical and Veterinary Entomology, 83: 141-158.

Entomophobia/Delusionary Parasitosis

Illusionary Parasitosis

ABSTRACT INTRODUCTION ENTOMOPHOBIA ILLUSIONS OF PARASITOSIS Definition Definition History History Psychopathology Psychopathology Treatment and Prognosis Treatment and Prognosis DELUSIONS OF PARASITOSIS Entomological Aspects Definition ACKNOWLEDGMENTS History REFERENCES Psychopathology Treatment and Prognosis Entomological Aspects

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This article titled "Insects in Psychiatry" was produced by Dr Phillip Weinstein of the University of Otago and originally appeared in the Digest of Cultural Entomology. Many thanks to Dr Weinstein for his kind permission in allowing this article to be included on our web site.

ABSTRACT Insects have profoundly influenced our culture through time, and it is therefore not surprising that they feature prominently in some psychiatric disorders. Historically, there has been considerable confusion and definitional overlap between insect phobias, delusions of parasitosis and illusions of parasitosis. Insect phobias involve an irrational fear of insects without the insect bites or infestation actually being experienced; whereas in delusions of parasitosis the patient believes that the bites or infestations actually occur. Illusions of parasitosis result from real environmental stimuli which are incorrectly perceived as being due to insects. Clinically, it is important to differentiate these conditions both from each other and from conditions with similar symptoms: the different psychologies involved should help direct appropriate treatment. INTRODUCTION Insects are an integral and influential part of our culture as illustrated by their infiltration of our language, arts, history, philosophy, and religion. However, as human society has become progressively more urbanized, insects have become progressively more estranged. As significant but increasingly intangible elements of our culture, insects now feature prominently in certain psychiatric disorders, much as do religious and extraterrestrial elements. Our perception of insects can range from appropriate apprehension when faced with the possibility of a bee sting, through subclinical and clinical insect phobias, to full blown psychotic delusions of insect attacks and infestations. We are concerned in this paper only with the clinical syndromes involving insects, since it is in this area that most confusion has arisen historically. Up until some twenty years ago most authors dealing with insects in psychiatry discussed several different syndromes under the same name. Authors are now increasingly aware of the distinctions bet-ween delusions of parasitosis, insect phobias, and illusions, but some overlap and confusion never the less remains. No paper to date has discussed these syndromes specifically to differentiate between them.

ENTOMOPHOBIA [Insect phobia; includes acarophobia (mites: scabies) and arachnophobia (spiders)]. Most people are at least wary, if not fearful, of certain insects (more correctly arthropods). This may be a reasonable fear based on knowledge or experience (bees, wasps, spiders, mosquitoes), an unreasonable but culturally understandable repulsion (cockroaches or flies), or a misplaced fear resulting from inadequate information (dragonflies, moths, crickets). A true insect phobia, on the other hand, is defined by the following criteria: Definition 1. A persistent irrational fear of and compelling desire to avoid insects, mites, spiders, or similar phobic objects; 2. Significant distress from the disturbance despite recognition by the individual that the fear is excessive or unreasonable; 3. Not due to another mental disorder such as schizophrenia or obsessive compulsive disorder (modified from DSM III 1980). The condition must be differentiated from delusions of parasitosis and illusions of parasitosis (following), and from obsessive compulsive disorder and schizophrenia. This can sometimes be difficult, even for an experienced psychiatrist. For example, the phobic object may be an insect infestation; that is, the possibility of becoming infested by ectoparasites is the feared notion, not the parasites themselves (as distinct from a delusion in which an imaginary infestation is actually experienced). A phobia of penetration/filth can also lead to cleaning and sterilizing rituals identical to those seen in obsessive compulsive disorder. As pointed out by Olkowski and Olkowski (1976), the syndromes satisfying these criteria represent only the tip on an iceberg, with much unnecessary avoidance behaviour never reaching a level where treatment is sought or necessary. History Although phobias probably occurred before recorded history, insects are less likely to have been phobic objects in the past. In hygienically urbanized western societies, many people have little first hand experience of insects other than flies and mosquitoes. Such urban societies are not as mentally or physically prepared for arthropod encounters as are rural communities (Coulson and Witter 1984). Psychopathology It is not unreasonable to assume that the danger and annoyance insects have caused to man over the millennia has resulted in an ingrained fear of insects in most societies. Bites and stings to humans and domestic animals act not only as stimulators of toxic and allergic reactions, but insects have been the vectors of potentially fatal diseases since prehistoric times. It is only very recently that such diseases as yellow fever and plague have come under control. Others, like malaria, remain a significant problem. An almost Jungian fear of insects can therefore be rationalized in all of us even if in the form of conditioned over-reactions. Fazio (1972) has suggested that the latter are largely a result of "vicarious learning family dependency" rather than of traumatic conditioning; most of his subjects lacked any real contact with the feared insects. Such explanations, however, are more likely to underlie the non-clinical end of the phobic spectrum than they are to underlie phobias satisfying the criteria set out above. In these clinical cases, as in other phobias, the more likely cause is a displacement of diffuse anxiety to an external focus which can be avoided. The choice of insects as the phobic object may be random, symbolic, or perfectly logical. When symbolic the insects often represent filth and soiling. They have also been interpreted as symbols of sexual penetration which cannot be eradicated (Schrut and Waldon 1963). The "logical" choice of insects as phobic objects is well described by Kolansky (1960). In a case of infantile neurosis and insect phobia involving a little girl, he describes how the symptoms resulted from her being told that her sister with pneumonia had died from a `bug.' Finally it is worth mentioning the interpretation of Savory (1964). He suggests that the fear of insects is a result of their rapid movements leading to retinal image movements similar to those involved in falling. Adrenaline release and an increase in muscle tone follow, and these are the factors which lead the brain to interpret `fright'- much like Jane Lange's theory of "feeling sorry because we cry." Treatment and Prognosis The role of the entomologist is primarily to dispel any possible misconceptions which may be exacerbating the phobia. Education here is a crucial element (for example to clarify the harmlessness of dragonflies). To put insects in a more positive light, and to remove such fears as may be passed on from parents, zoos and museums can play an integral educational role. The live insect exhibit at the Los Angeles Natural History Museum is an example: volunteers take insects from their cages and hold them out for visitors to fondle - which most children do (Mofet 1979). Specialist treatment will be as for other phobias, and is largely determined by the therapist's individual preferences. Methods reported in the literature include supportive psychotherapy, esensitization (Fazio and Erk 1973), insight psychotherapy, combination of therapies (possibly including group therapy), drug therapy (anxiolytics), modelling (Denney and Sullivan 1976), hypnotic regression and reframing (Domangue 1985), and implosive therapy (Fazio 1972). For chronic phobias the prognosis is good if the underlying conflict can be dealt with. If the conflict is deep and exhibits symbolic elements, the prognosis is worse, and the presence of compulsive symptoms such as cleaning makes it worse still (cf. delusions of parasitosis). Entomological aspect most medical graduates will have a basic knowledge of entomology, and will be able to reassure patients about the harmlessness of phobic objects such as dragonflies and moths. Reference to a basic entomology text, or a quick call to an entomologist, should be encouraged to help clarify any detailed misconception that may be contributing to the phobia. It is useful to remember that only blood feeders (mosquitoes, fleas, ticks, bedbugs) actively pursue humans. The more common phobic objects (spiders, bees) never bite or sting unless trapped or seriously threatened. Although the former category comprises insects which are associated with poverty or poor sanitation, insects in the latter category, which are beneficial to man, are feared the most (Olkowski and Olkowski 1976).

DELUSIONS OF PARASITOSIS [Ekbom syndrome, monosymptomatic hypochondriasis, formication]. Although rarely mentioned in textbooks of psychiatry, and not classifiable in DSM III (Maier 1987), many European authors feel that `monosymptomatic hypochondriasis' deserve their own diagnostic label (Bishop 1980 and references therein). The syndromes include dysmorphophobia, olfactory reference syndrome, and, most prominently, delusions of parasitosis. Ekbom (1938) was the first to clearly differentiate the syndrome from entomophobia, and his name is often used eponymously therewith. He used the term Dermato-zoenwahn, which is still current in the German literature (Musalek et al. 1988). For English speakers, the term delusions of parasitosis, first used by Wilson and Miller (1946) appears to be the most appropriate, unless one has a penchant for eponyms. Definition An unshakable false belief that live organisms are present in the skin (Obermeyer 1961). These organisms range from insects to worms and bacteria (Wilson and Miller 1946), the type often depending upon the parasitological knowledge of the patient. It is important to note that delusions of parasitosis may be a symptom complex rather than a disease entity, as it is found in a variety of physical and mental diseases; nevertheless, it is often the only recognizable abnormal element. Where the delusion of parasitosis is not the major symptom, as in Delirium Tremens, it may be better to use the term `formication.' In this way, delusions of parasitosis should eventually become restricted to a single disease entity (or disappear from use) as our nosological knowledge increases. Maier (1987) suggests that the reines Dermatozoenwahns (true delusions of parasitosis) may be those not involving organically based diseases or schizophrenia. In his original description, Ekbom himself did not include delusions of parasitosis which were part of complex frame works, only those in which delusions of parasitosis were the sole psychiatric symptom (i.e. primary delusions). The condition must be differentiated from entomophobia (above). Similar symptoms may occur in a number of other conditions which, as discussed, are perhaps best otherwise classified (drug induced organic brain syndrome (Bishop 1980, Bourgeois et al. 1981, Todd 1968), schizophrenia, factitial dermatitis, manic depressive psychosis). The most important diagnostic consideration is an awareness of the fact that patients with delusions of parasitosis experience the state of being infested. This is fundamentally different from having a fear of becoming infested, which falls into the category of entomophobia. This distinction has not been made clearly in the literature and is often a source of confusion between phobia and delusion (e.g. Galeota 1966). The phobia immediately entails a better prognosis, as reality testing remains unimpaired. History The earliest well documented case appears to be that described by Thibierge(1894), although he applied the term "Acarophobe." The case is clearly one of delusions of parasitosis according to Ekbom's later (1938) definition. Psychopathology An obsessional, anankastic personality is a predisposing factor in most suffers (Bourgeois et al. 1981), and female cases are most frequently reported (Berrios 1985, Wilson and Miller 1946). The syndrome is often preceded by an original and very real arthropod infestation acting as a `trigger' (Schrut and Waldron 1963). Senile pruritus or other tactile sensory disorders may also act as triggers, which become elaborated into a delusion and are later `fixed' (Wilson and Miller 1946, Berrios 1985). Possible triggers therefore also include systemic disease (diabetes, TB, syphilis) and deficiency states such as pellagra. These disorders (as well as real infestations!) must obviously be identified in order for treatment to be appropriate. Presenting complaints include itching, biting, stinging, burning and crawling sensations. Insects are often described as black or white, jumping, and sometimes emerging from cosmetics or toothpaste (Waldron 1962). The `matchbox' sign, where the patient brings specimens at the first visit, is ominous. Microscopic examination of the contents usually reveals only lint, scabs, or other household dust. Such negative findings invariably lead to more intense collection and presentation of specimens (Schrutt and Waldron 1963). One can often elicit a list of attempted treatments including all imaginable varieties of detergents, balms and poisons. More rarely, the presenting complaint is one of auditory hallucination (Wilson and Miller 1946). Patients most commonly present to dermatologists (if skin changes are present) or pest control officers (if they are not). In the former case excoriations are classically produced by the fingernails and there may also be signs of chemical burns as a result of attempts to kill the parasites. The patient is compelled to dig the parasites out, especially before going to bed, and often resorts to the use of a knife, tweezers or other sharp implement, leaving skin lesions consistent therewith. For those patients presenting to pest control officers, Gage (1957) and Galeota (1966) both warn of the risk of making treatment even harder by `fixing' the delusion with reinforcing statements or insecticide applications. The symptoms may be carried over, or passed on by suggestion, to other members of the family. Folie � deux occurs with a surprisingly high frequency. If a disease entity delusions of parasitosis exists per se, it may well lie within this category as a primary delusion (Evans and Merskey 1972). Treatment and Prognosis Delusions of parasitosis are far more common than is indicated by the literature: almost every dermatologist knows of a couple of cases (Bourgeois et al. 1981), as do most entomologists and pest control officers (Galeota 1966, Gage 1957, Weinstein pers obs.). Despite such an apparent frequency of affliction, there is no generally accepted approach to treatment, with many therapists (perhaps reasonably) adopting the attitude that "some treatment, scientific or foolish, which the patient can be made to apply with confidence, will bring about some relief" (Smith 1934). Psychotherapy and psychoanalysis have been successful in treating delusions of parasitosis associated with repressed conflicts over sexuality and aggression (Torch and Bishop 1981) and drug treatment with pimozide can provide significant relief of both itch and delusions (Hamann and Avnstorp 1982). A number of other treatments, including ECT, are used less frequently or have fallen out of favour. There is an ongoing debate as to whether dermatologists or psychiatrists should treat patients with delusions of parasitosis. Dermatologists often argue that although psychiatrists are better qualified to deal with the delusions, the nature of the patients is such that they are likely to be lost to treatment should a psychiatrist be mentioned. It is therefore better for the dermatologist to maintain treatment on pimozide for example, than it is for the patient not to be treated at all (Hahmann and Avnstorp 1982). A good dermatologist should ideally be able to present the "second opinion" sought from the psychiatrist in such a way as to not loose the patient to further treatment. Obermeyer (1961) suggests that the dermatologist screen and refer sufferers along the following lines:  Depression or psychosis present - immediate referral to a psychiatrist;  Patient recognizing emotional involvement - referral to psychotherapist;  Patient denying emotional involvement and hostile to psychiatric concepts - supportive or drug therapy administered by dermatologist. The prognosis is very variable, and often dependent on those other diagnosed or undiagnosed disease complexes which contribute to the symptomatology. The formication of Delirium Tremens for example has an excellent prognosis, but it is worse in schizophrenia and affective disorders. The prognosis is very poor in paranoid conditions since these assessments are usually not suitable for psychotherapy/analysis. Obermeyer (1961) describes paranoiacs who would dig into their skins "up to the time of involuntary parting, and who probably still dig, under somebody else's auspices"! Entomological Aspects Although most therapists will see patients who have already been screened for genuine infestations, anyone involved with the case has the responsibility to ensure that another dermatologist or parasitologist rechecks negative findings if any doubt whatsoever exists. Despite the presence of personality traits or psychiatric symptoms which corroborate a diagnosis of delusions of parasitosis, the patient is sometimes infested. The reader is referred to a paper by Traver (1951) where she describes her suffering through a seven year infestation by the mite Dermatophagoides schermetewskyi Bogdanow. Unlike Sarcoptes scabei which is easily located in epidermal burrows, this beastie inhabits the dermis, and could not be found. The response of the physicians she consulted was quite predictable when Traver presented with formication, classical self induced excoriation, a history of trying a long list of chemical remedies, and two adult female family members living with her with identical symptoms. The details of natural history related by patients are often quite complex (Miller 1954), and depend upon the patients' previous entomological knowledge. Imagined animals range from fleas, lice and scabies through itch-mites, bedbugs and worms, to nondescript "black things" and insects new to science (Wilson and Miller 1946). In assessing the feasibility of the details related by the patient, it is important to compare these with existing knowledge. A rudimentary understanding of arachnid life cycles, biology and behaviour, if not already known, is easily obtained by any therapist by consulting medical entomology texts or local entomologists. Remember that psychiatric patients can be the unwilling hosts of lice, mites, and bedbugs as easily as can anyone else.

ILLUSIONS OF PARASITOSIS Definition Unlike delusions of parasitosis, illusions of parasitosis result from actual environmental stimuli (Heidbreder and Waldron 1971). The stimuli are incorrectly interpreted and are attributed to insects or other small organisms which are then thought to be biting or infesting the person, their home, and/or their working environment. Illusions of parasitosis are particularly common in groups. Their "contagious" nature parallels the high incidence of folie � deux in delusions of parasitosis, and although not a psychiatric disorder per se, an awareness of such illusions may help to explain `triggering,' suggestive cross infection, and psychological enhancement of both insect phobias and delusions of parasitosis. Illusions of parasitosis can be readily differentiated from both entomophobia and delusion of parasitosis by considering a few simple questions as outlined in the following table (adapted from Waldron 1972). History The phenomenon was first studied seriously in the context of "mass entomophobia" due to "cable mites" and "paper lice" in offices and laboratory environments in the 1960's. The subject borders on forensic entomology: see for example the classic account of how dermatitis caused by a persistent laboratory infestation of "cable mites" was eventually eliminated when rockwool aerosol was recognized as issuing from the laboratory air-vents (Scott and Clinton 1967). Today, such a case would undoubtedly have resulted in several law suits. Psychopathology Possibly the most notable aspect of illusions is the ease with which symptoms are transmitted. Dermatitis, itching, formication and bites (in this case obviously proportional to the causative stimulus) are the most common symptoms, and, in co-workers, a phobia of being affected. Over one hundred and fifty people may be affected simultaneously, the symptoms also being transmissible to unaffected individuals by suggestion. Females are most commonly affected, and associations are often made between the symptoms and personal office problems, leading to an overall loss of morale and efficiency. Environmental factors may be predisposing, such as a poor working environment, dull routine work, or too much pressure. Apart from obviously physical agents such as the rockwool mentioned above, the genesis of an outbreak has been broadly attributed to both transposition of symptoms and transmission by suggestion. Transposition of symptoms may follow a true or triggering infestation, such as fleas at home. Resulting bites may be associated with a situation at the office, and the problem is thus transposed from one environment to another (Waldron 1972). Transmission of symptoms (e.g. itching) from one person to another may take place if the symptoms are in turn associated with the second person's own personal office problems (ibid). The symptoms are often further exaggerated for secondary gain. Treatment and prognosis As with delusions of parasitosis, the importance of excluding a true entomological cause cannot be over-emphasized. An experienced pest- control officer or competent industrial epidemiologist should be consulted. In my own former laboratory, several people including myself were repeatedly and frustratingly bitten by something we could not locate for many days. "Starling lice" (Ornithonyssus sp. - a mite) were the cause, and pigeon and starling nests were subsequently removed from the eaves of the building. Non-entomological causes may be identified with the help of some detailed detective work, as in the case of Scott and Clinton's "cable mites" (1967). The therapist's role is to be aware of the possibility of such illusions in the context of their interactions with the disorders discussed previously. In the absence of complicating factors, the illusions obviously resolve once the physical stimulus is identified and eliminated. Symptoms are also substantially alleviated by action taken in deference to the psychological state of the workers, such as their working environment, chores and work pressure (Scott and Clinton 1967). Entomological Aspects "Cable mites" and "paper lice" are non-existent entities. Those arthropods which are potential pests to man have well defined behaviour and habitat requirements, all of which can be discovered in medical entomology texts or in consultation with local entomologists. A comparison of known facts to reported complaints will, as in the delusions of parasitosis, tend to support or reject the involvement of insects or other arthropods. Entomological effects of psychiatric conditions Although entomological effects of psychiatric conditions cannot be considered significant in the current context, they are mentioned here for completeness and for interest. Coulson and Witter (1984) classify human responses to arthropods in 5 categories. When confronted with insects or damage they have caused people either: 1. Go hysterical - i.e. exhibit entomophobia; 2. Go on a killing spree ("the only good insect is a dead insect"); 3. Tolerate the insects and plant damage once they understand that no serious or permanent harm can be done; 4. Are indifferent or do not respond; 5. Go `environmental', protect living things, and denounce all insecticides and repellents. Which response is likely depends upon the person's knowledge and experience as well as the type and number of insects. At a community level, the uninformed extrapolations made from germ theory have resulted in excessive `cleanliness,' with overuse of insecticides, elimination of natural predators, and development of insecticide resistance (Olkowski and Olkowski 1976). At an individual level, the more interesting cases arise, such as the traditional example of the arachnophobic man who obsessively killed every spider in his house and garden. Having removed all predators, the pest resurgence in his vegetable patch was phenomenal! My favourite case report is that of an Irish woman who passed thousands of coprophagous beetles of the genus Blaps in her stools. She presumably ingested eggs or larvae inadvertently when she ate clay and chalk taken from the graves of priests (Westwood 1839, cited in Matthews 1975)! Fortunately, people with entomologically oriented psychiatric disorders are (arguably) not frequently in positions of political or economic power, and such people do not therefore affect insects in the ecological sense.

ACKNOWLEDGMENTS I [Phillip Weinstein] wish to thank the late Charles Hogue for his early encouragement in pursuing this topic, and Dexter Sear for subsequently facilitating the project. Jack White helped with references and Agnes Feld typed the manuscript.

REFERENCES Berrios, G.E. (1985). Delusional parasitosis and physical disease. Comprehensive Psychiatry. 26: 395-403. Bourgeois, M., J.M. Amestov and J. Durand (1981). D�lires d'infestation, dermatozooes et ectoparasitoses d�lirantes, syndrome d'Ekbom. Ann. Med. Psychol (Paris) 139: 819-828. Bishop, E.R. (1980). Monosymptomatic hypochondriasis. Psychosomatics 21: 731-747. Coulson, R.N. and J.A. Witter (1984). Arthropod pests in recreational areas. In: Forest Entomology. John Wiley & Sons, New York. Ekbom, K.A. (1938). Der praesenile Dermatozo-enwahn. Acta Psychiatr. Neurol. Scand. 13: 227- 259. Evans, P. and H. Merskey (1972). Shared beliefs of dermal parasitosis: Folie partag�e. Br. J. Med. Psychol 45: 19-26. Denny, D.R. and B.J. Sullivan (1976). Desensitization and modeling treatments of spider fear using two types of scenes. J. Cons. Clin. Psychol. 44: 573-579. Domangue, B.B. (1985). Hypnotic regression and reframing in the treatment of insect phobias. Am. J. Psychotherapy. 39: 206-214. DSM III (1980) Quick reference to the diagnostic criteria from DSM III. American Psychiatric Association. Fazio, A.F. (1972). Impulsive therapy with semiclinical phobias. J. Abnor. Psych. 80: 183-185. Fazio, A.F. and T.W. Erck (1973). Components in a treatment of insect phobias. J. Abnoral Psychol. 82: 463-468. Gage, R.W. (1957). What to do about insect phobias. Pest Control. (Oct) 42-7. Galeota, W.R. (1966). Entomophobia and what it means to a PCO. Pest Control. (Jan) 17-18. Hamann, K. amd C. Avnstorp (1982). Delusions of infestation treated by Pimozide: A double-blind crossover clinical study. Acta Dermatovener (Stockholm) 62: 55-58. Heidbreder, G.A. and W.G. Waldron (1971). Illusions of parasitosis. Letter to Editor, JAMA, June 28, 216: 2145. Hopkinson, G. (1973). The psychiatric syndrome of infestation. Psychiatr. Clin. 6: 330-345. Hogue, C.L. (1987). Cultural entomology. Ann. Rev. Entomol. 32: 181-99. Kolansky, H. (1960). Treatment of a tree-year-old girl's severe infantile neurosis. Psychoanalytic Study of the Child 15: 261-285 Maier, Ch. (1987). Zum Problem des Dermatozoenwahnsyndroms. Nervenarzt 58: 107-115. Matthews, E.G. (1975). The Mediterranean beetle Blaps polychresta Forskal in South Australia. The South Australian Naturalist. 49: 35-39. Miller, L.A. (1954). An account of insect hallucinations affecting an elderly couple. Can. Entomol. 86: 455-7. Moffet, B.S. (1979). Even creepy bugs useful, ex-pert says. Los Angeles Times, Thurs, 30, Part 1-C 7. Musalek, M., J. Gr�nberger, O.M. Lesch, L. Linzmayer, H. Walter und W. Gebhart (1988). Zur Psychopathologie der Dermatozoenwahnkranken. Der Nervenarzt. 59: 603-609. Obermayer, M.E. (1961). Dynamics and management of self-induced eruptions. California Medicine 94: (2) 61-65. Olkowski, H. and W. Olkowski (1976). Entomophobia in the urban ecosystem, some observations and suggestions. Bull. Entomol. Soc Am. 22: 313-317. Savory, T. (1964). Arachnida. Academic Press, London and New York. Schrut, A.H. and W.G. Waldron (1963). Psychiatric and entomological aspects of delusory parasitosis. J. Am.Med.Assoc., 186: 213-214. Scott, H.G. and J.M. Clinton (1967). An Investigation of "Cable Mite" dermatitis. Annals of Allergy. Vol 25, No.8.Smith, R.C. (1934). Halluci-nations of insect infestation causing annoyance to man. Brooklyn Ento. Soc. Bull. 29: 208-212. Thibierge, G. (1894). Les acarophobes. Rev. Gen. Clin. Ther. 32: 373-376. Todd, J. (1968). Lilliputian hallucination complicating dexamphetamine-amylobarbitone addiction. Br. J. Addict. 63: 271-274. Torch, E.M. and E.R. Bishop. (1981). Delusions of parasitosis in psychotherapeutic engagement. Am. J. Psychother 35: 101-106. Traver, J.R. (1951). Unusual scalp dermatitis in humans caused by the mite Dermatophagoides. Ent. Soc Washington 53: 1-25. Waldron, W.G. (1962). The Role of the entomologist in delusory parasitosis (entomophobia). Ento. Soc. America Bull. 82: 81-83. Waldron, W.G. (1972). The entomologist and illusions of parasitosis. Calif. Med. 117: 76-78. Westwood, J.O. (1839). An introductin to the modern classification of insects. Longman, Orme, Brown, Green and Longmans, London. Wilson, J. W. and H. E. Miller (1946). Delusion of parasitosis. Arch. Dermatol. 54: 39-56.

Exotic Myiasis  Introduction  Natural History  Myiatic flies - Diagnosis  Clinical Presentation & Treatment  Quarantine Considerations  References  Confirmation and Enquiries modified from: K.G.V. Smith (ed). 1973. Insects and Other Arthropods of Medical Importance. British Museum, London.

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Introduction Myiasis is the invasion of living tissue or organs by the immature stage (maggots) of flies. Every year several species of exotic diptera are imported into Australia in the subdermal layers of the skin of overseas travellers. Patients returning from overseas present to their doctor with painful furuncular lesions, often unaware that the cause is a maggot.

Natural History In Australia, the exotic species of fly isolated from patients with travel history include the human bot fly (Dermatobia hominis), the Tumbu fly (Cordylobia anthropophaga), the Lund's fly (Cordylobia rodhaini) and the New World screw worm fly (Cochliomyia hominivorax) (Table 1). Each species has an interesting life cycle, but the human bot fly D. hominis is especially unique. The eggs of D.hominis are couriered to the host by a blood sucking insect, such as a mosquito. After the young larvae penetrate the host's skin, they feed continuously for 5-12 weeks from a dermal pocket, causing severe pain and intense pruritus to the host. At the prepupal stage, they fall from the host to pupate

Fig. 1 Larval Cordylobia rodhaini, note the scattered spines. Bar = 1mm. in the ground. In its native home of Central and South America, D.hominis regularly infests humans and a wide range of animal hosts, especially cattle. This fly's distribution extends from Mexico through Central and South America down to northern Argentina and Trinidad. Both species of Cordylobia are found only within the African continent. The Tumbu fly is a common blowfly of tropical Africa, south of the Sahara Desert. The Lund's Fly is a blowfly rarely involved in human myiasis (Zumpt, 1965); it is found in rainforest areas of tropical Africa, from Senegal to Central Africa and south to Angola and Rhodesia, usually associated with rodents. Females of these two Cordylobia species deposit their eggs below the surface of sandy soil and occasionally on clothing that has been tainted with traces of faeces or urine. Any disturbance of the soil surface is met with an immediate response from the young larvae that wriggle to the surface in order to penetrate the skin of the host. The life cycle of the two Cordylobia species takes 10-12 days to develop to the prepupal stage, when it leaves the host to pupate. Within this time the patient will endure pain and intense itching from the developing lesion.

Fig 2. Larval Dermatobia hominis, note the rows of spines. Bar = 1mm.

The New World screw worm (C.hominivorax), is a species of maggot that can burrow into the flesh of humans, wild and domestic animals. Where it was once more widespread in its distribution it is now generally limited to Central and South America (Kettle, 1995). Females of this fly species deposit their eggs on the edges of wounds, sores and healthy mucous membranes. After burrowing into the host’s tissue, the young larvae feed on living tissue for 4-8 days. This causes extreme pain and disfunction to the host from the festering wounds before the maggot matures to the prepupal stage when it leaves the host.

Myiatic flies - Diagnosis

Species of diptera Country of origin Incubation period Appearance of mature maggot

Cochliomyia Central & South 4-8 days Typical maggot shape, 15-17mm long, bands hominivorax America of spines encircling anterior margin of each body segment.

Cordylobia Central & Tropical 10-12 days Oval, 11-15mm, 3 curved slits in spiracles, anthropophaga Africa numerous small black spines.

Cordylobia rodhaini Central & Tropical 10-12 days Up to 23mm long, scattered spines, 3 (Fig. 1) Africa sinuous slits in each posterior spiracle.

Dermatobia hominis Central & South 5-12 weeks 18-25mm long, pair of flower like anterior (Fig. 2) America spiracles, spines in rows.

Clinical Presentation & Treatment Infections with myiatic flies start out as itchy sores that then develop into painful boil-like lesions, which often ooze. Most of these cases of human myiasis are uneventful, but patients should be monitored for additional and subsequent lesions as the development of the maggots is not synchronous or isolated, and their growth phase may be prolonged. Treatment of this condition can be undertaken by forcing the maggots to the skin's surface by cutting off their air supply. An application of Vaseline or similar material will encourage the maggot to move towards the surface exposing more of the maggot's body that can then be extracted. A local anaesthetic and incision to extract the maggot is another common method of treatment.

Quarantine Considerations Although imported cases of exotic myiasis are not notifiable in Australia, they demonstrate the ease at which these flies cross geological boundaries with air travel. As there are no obligatory fly parasites of humans in Australia, these cases of exotic myiasis are a constant reminder of the problems in other countries. Awareness of exotic myiasis by health professionals would assist quarantine, agriculture and other departments in monitoring the different species entering Australia. Establishment of any one of these pest species of fly would have disastrous effects on our health and agricultural industries and economy.

References Kettle, D.S., 1995, Medical and Veterinary Entomology. CAB International, Wallingford, UK. Zumpt, F., 1965, Myiasis in Man and Animals in the Old World. London, UK.

Confirmation and Enquiries Identification of myiatic flies, and all other medically important insects, is performed through the Medical Entomology Department at ICPMR, Westmead Hospital.

Fleas  Natural History  Clinical Presentation  Laboratory Diagnosis  Treatment and Control  Confirmation and Enquiries

modified from: Kettle, D.S. (1995). Medical and Veterinary Entomology. CAB International. Wallingford

bottom of page Natural History Fleas are highly specialised bloodsucking parasites belonging to the order of insects called Siphonaptera, which means "wingless siphon". They have a formidable reputation of claiming more victims than all the wars ever fought, as a result of the "bubonic" (Black Death) plague they spread throughout the world in the 14th century causing the deaths of over 200 million people. Now, these insects are better known for their irritation and pest status worldwide. Fleas are light brown to mahogany in colour and roughly oval shaped. Their laterally flattened appearance enables them to quickly move through the host's hair. Measuring 2-8 mm in length, the adults are entirely covered with a series of bristles and combs that assists them in clinging to the host. The small head is equipped with sawing and sucking mouthparts, and two tiny simple eyes. To aid in the detection of a host, fleas possess two short antennae on the head that are sensitive to stimuli including heat, vibration, traces of carbon dioxide and change in air currents and shadows. The hind pair of legs that are well developed for jumping enable fleas to be propelled 10- 30cms, either to make contact with a host or avoid a threatening situation. Both female and males fleas rely on blood for their nutrition, but can survive for several months without it. When a flea blood feeds, it will crouch low to penetrate the host's tissue with a sawing motion of the mouthparts. A small amount of anti-coagulatant is injected with the saliva, to permit easy siphoning of the blood. Fleas will bite only accessible parts of the body and clustered bites on the lower limbs are diagnostic. Blood feeding maybe interrupted, and fleas will often probe several times before repletion which can increase their total body weight by 30%. Each female flea uses her blood to nourish developing eggs, and will deposit up to 4 eggs after each blood meal; most females will lay at least 100 eggs within a life cycle of several months. The eggs are oval, white to cream in colour and measure 0.5mm in length; they can hatch within 1 week, but this will be dependent on prevailing conditions as larvae are extremely sensitive to desiccation. When the maggot-like larvae emerge, they are sparsely covered in hair and have no legs but are capable of moving rapidly in search of food, which consists mainly of skin scales or undigested blood excreted by the adults. Within a 1-3 week period, the larvae will grow and undergo 4 moults prior to pupating in a silken cocoon which they spin. The adult fleas emerge from the pupal case in 1-2 weeks but can remain dormant in their cocoons for several months depending on the availability of food and conditions. Often the emergence of adults from the pupal stage is triggered by vibrations, which occasionally happens on entering an unoccupied home of previous pet owners.

Clinical Presentation Some fleas can attack a range of hosts, and their ability to transfer from one host to another allows for the possible transfer of pathogens including viral, bacterial and parasitic diseases. The main flea species that attack humans include the cat flea Ctenocephalides felis, the dog flea C. canis, and the human flea Pulex irritans. The latter two species are relatively rare. The common cat flea is found on both cats and dogs, and is the species usually identified in attacks on humans and usually responsible for flea plagues. Cat fleas are the intermediate host for the dog and cat tapeworm (Dipylidium caninum) which is easily transmitted to humans. The only flea-borne disease that currently occur within Australia is murine typhus; this is transmitted from rats to humans by particular rat fleas, typically Xenopsylla cheopis, and although it has been widespread, it is uncommon. The continual biting activity of fleas alone causes a great deal of irritation and distress to humans, especially during flea plagues. Reactions to the flea's saliva are often delayed, with the formation of a wheal surrounding each puncture site within 5-30 minutes of the bite, accompanied by intense itching. Within 12-24 hours each wheal may progress to a small lesion or vesicle. The onset of symptoms in sensitized individuals often develops much later, and the initial reaction may become apparent only after 12-24 hours. Fleas are the major cause of papular urticaria, particularly on the legs of children, and continual scratching may lead to secondary infections.

Laboratory Diagnosis Identification of fleas is performed with the use of light microscopy and taxonomic keys.

Treatment and Control With the increase in carpeted homes, central heating and number of household pets, flea control is a continuing problem for pest controllers and pet owners. The prolonged periods of warm, humid weather in the summer months provide ideal conditions for fleas to flourish. Typically, concentrations of the immature stages of fleas (eggs and larvae) will be found in areas where pets feed and rest, and control measures should be targeted at any such areas, in addition to their housing, basket, blankets and the pets themselves. Regular vacuuming of floors and washing of pets and bedding with an insecticidal preparation will aid in control. Newer products with insect growth regulators are (e.g. in aerosol "bombs") are readily available in supermarkets provide an economical means of eradication by fumigation of a home, but they should only be used as directed.Continual reinfestation of fleas in homes may indicate the source has not been detected and may require intervention by a reputable pest controller.

Confirmation and Enquiries Identification of fleas and all other medically important arthropods is preformed through the Medical Entomology Department at ICPMR, Westmead Hospital.

Head Lice

 Natural History  Clinical Presentation  Laboratory Diagnosis  Treatment and Control  Confirmation and Enquiries  Links

modified from: Kettle, D.S. (1995). Medical and Veterinary Entomology. CAB International. Wallingford

bottom of page Natural History Head lice (Pediculus capitis) are blood sucking ectoparasites of humans from the family of lice Pediculidae, and they have world wide distribution. This common human parasite is strictly host specific and does not affect other animals. An adult head louse is a small six legged insect, 2.5-3.5mm in length, with well developed eyes, small antennae and a flattened light brown body which is slightly lobed at the margins. The claws on each leg enable the lice to hold on to hairs, and they can run quickly over the scalp through hair. Head lice live their entire life (about a month) on the head of their host, and are often concentrated towards the back of the head and above/behind the ears. All nymphs (immature stages) and adults blood feed on the surface of the scalp until fully engorged, and can feed at any time of the day or night. A female head louse can lay 6-8 pale coloured oval shaped eggs (or nits) a day, and may lay 300 eggs within her lifespan. The eggs are glued to the base of the hair shaft and grow out with the hair. The further away from the scalp that eggs are found can be an indicator of the length of the infestation (and most eggs found further than 1cm from the scalp should be hatched or are dead). Most eggs hatch within 7-10 days but some can remain unhatched for up to 3- 4 weeks. Individuals who have a head louse infestation will have on average 10-20 lice at any given time. Without a bloodmeal and the humid environment their human host provides, head lice will only survive a few days. They cannot infest furniture, bedding, pets or other household situations - they must have a human host. Transfer of head lice to individuals is by hair to hair, head to head, close bodily contact. Sharing combs, brushes, ribbons, hair bands, hats, pillows and similar personal articles is the other main way that lice can spread. Lice will not voluntarily leave the scalp. Head lice tend to be more common among children than adults, and do not discriminate between sex or hair colour - although lice in lighter coloured hair may be more difficult to detect. Head lice do not prefer dirty or unkempt hair, but may go unnoticed and proliferate in such an individual compared with one who pays attention to their hair. However, an infestation should not be seen as a reflection on personal hygiene, home environment or social status, and should not be seen as a social stigma.

Clinical Presentation An infestation of head lice may not be noticed initially, but with time will produce irritation leading to scratching of the scalp. Persistent scratching can cause development of lesions which may give rise to secondary infections and, in some cases, even swollen lymph glands. Lice are a nuisance and can disrupt people’s rest, but they are not responsible for the spread of any infectious disease-causing organisms. The detection of eggs of the shaft of the hairs is the most common method of identifying a head louse infestation, and it usually indicates the lice have been established for some time. In addition to observing the lice throughout the hair, further evidence of head lice may be seen on pillows or bed linen in the form of dark powder (faeces of the louse) or cast skins. Heavy infestations of head lice, if left untreated, result in matted hair interspersed with lice, their cast skins and faeces, plus attached eggs and egg shells, and may eventually eventually develop a putrid odour.

Laboratory Diagnosis Identification of louse specimens is by light microscopy. Details from the patient on exactly what part of the body the specimens were collected is important in establishing the identity of the louse. The body louse, Pediculus humanus (see Body Lice), is taxonomically impossible to differentiate from the head louse, but body lice are never found on the head (they are most often in the clothing where they lay their eggs attached to cloth fibres) and head lice are generally not found on other parts of the body. Pubic lice, Pthirus pubis (see Pubic Lice), are typically found in the pubic and perianal areas but are occasionally found in hair on the trunk and head, including the beard and eyelashes.

Treatment & Control Head lice are contagious and infect a large number of school age children annually. When a case of head lice is detected the person should be treated immediately with a preparation obtained from a pharmacy. A wide range of liquid products (and fine toothed combs) are available and a prescription is not necessary. Products with permethrin or malathion are usually recommended. One or perhaps two applications are advised and all family members, and other close contacts, should be treated at the same time. The presence of unhatched nits or eggs after the preparation has been applied is not necessarily a sign of treatment failure - the treatment will not separate eggs from hairs, they must be physically removed - but the presence of living lice indicates either a treatment failure or a reinfestation. A combined effort by school authorities requesting parents to treat all children in affected classes over a weekend will decrease the incidence of reinfestation. The control measures should be widespread to be effective and limit the risk of re-infestation. If re-infestation occurs it may indicate that not all infestations have been found and treated. Repeated finding of lice in some individuals following treatment could be a sign of resistance of head lice towards the chemical preparation, but there is little evidence for the presence of resistance in Australia, and inadequate treatment and opportunities for reinfestation should first be considered as an explanation. Some people may experience itchiness after a treatment but they should be careful to not automatically suspect persistence of lice, and should not automatically reapply the anti-lice products to relieve their discomfort. Routine or repetitious use of these preparations is unwarranted and expensive, and can lead to further irritation and other skin problems.

Confirmation and Enquiries Identification of head and other lice, and all other medically important insects, is performed through the Medical Entomology Department at ICPMR, Westmead Hospital. See 'Contacts' for further information.

Related Links (Extensive review on headlice and its treatment from Richard Pollack, Harvard University). (The American National Pediculosis Association, headlice information). (School IPM WWW site; details methods of pest management relevant to schools with an excellent presentation on headlice in Powerpoint format).

Japanese Encephalitis virus Overview Natural History Symptoms Laboratory Diagnosis Treatment Prevention Further Reading

bottom of page Overview Japanese encephalitis virus is a mosquito-borne virus which is potentially fatal in humans. It is spread throughout eastern Asia, including India, Japan, China and southeast Asia. The virus made its appearance in Australia for the first time in 1995, when three residents of Badu Island in the Torres Strait developed clinical disease and two died. Antibodies in humans and pigs were demonstrated on other islands, and JE was isolated from Culex annulirostris collected on Badu Island. In late 1995, 93% of humans in the region of activity were vaccinated. Serological evidence that transmission had occurred in pigs in 1996 and 1997 followed, as did evidence that JE virus has been in PNG for eight or more years and has spilt over into the Torres Strait islands in the past four years: in 1995 into humans, in 1996 and 1997 into pigs, and in 1998 into humans and pigs. In March 1998, a boy from the island of Badu was hospitalised with JE infection, indicating renewed activity in the region; the boy came from a religious group that had refused vaccination during the 1995 campaign. Later the same month, a professional fisherman was infected while in the Mitchell River area on the western side of Cape York Peninsula; this was the first case of JE infection acquired on the mainland of Australia (seropositive pigs have also been detected in the Mitchell river area). Both patients recovered.

Natural History The natural cycle of Japanese encephalitis (JE) virus in Asia involves water birds and Culex mosquitoes, particularly Cx. tritaeniorhynchus, with pigs being also involved as an amplifying host and providing a link to humans through their proximity to housing. In the Torres Strait outbreak, Cx. annulirostris was found to be infected and is presumed to be the principal vector. If JE virus was to continue activity in the region, it is likely that it could become established on the mainland further south, and could present a major problem in areas where Cx. annulirostris is abundant.

Symptoms, Diagnosis, Treatment Symptoms of infection are similar to those described for Murray Valley Encephalitis (MVE) virus, and JE virus has a comparable mortality rate of 20-30%. Likewise, the diagnosis and treatment are essentially the same, although specific JE virus antibodies are tested for in the blood tests.

Prevention A vaccine is available to prevent infection and available through clinics that specialise in travel medicine. Individuals who travel to Asian countries should consult a travel medicine clinic on the need for vaccination. General mosquito avoidance measure as per MVE are also advisable, including the use of insecticide impregnated nets when sleeping in rural areas.

Further Reading Burke, D.S. and Leake, C.J. (1988). Japanese Encephalitis. in Monath, T. (ed). The Arboviruses: Epidemiology and Ecology, Volume III. CRC Press, Florida, pg: 63-92.

Lyme Disease

LYME DISEASE IN BACKGROUND AUSTRALIA Introduction History - Australia Ecology Clinical Investigations Clinical Features Serological Investigations Vector and Reservoir Host Diagnosis - Culture/PCR Investigations Diagnosis - Serology Conclusions - Australia Treatment Summary Prevention Further Reading/Links

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BACKGROUND Introduction Lyme disease (LD) is a tick-borne zoonosis caused by the spirochaete bacterium, Borrelia burgdorferi. Since the disease was first recognised in 1975 it has become the most frequently reported human tick-borne infection worldwide. It has been reported from every continent (except Antarctica) although doubt remains as to whether it occurs in the southern hemisphere in general, and in Australia in particular. Ecology LD is transmitted to humans by ticks. Larval and nymphal stages feed on infected reservoir hosts, acquire the organism and then, after moulting to the next life stage (nymphs and adults respectively), pass on the infection to humans and other animals. In the northern hemisphere, small placental mammals are reservoir hosts. The only species of ticks shown to be competent vectors of B.burgdorferi to humans belong to the Ixodes persulcatus complex, including I. scapularis and I. pacificus in the United States, I. ricinus in western Europe, andI. persulcatus in eastern Europe and Asia. No species of this complex exist in Australia.

Clinical Features The epithet "The Great Imitator" is now used for LD as it was once for another major spirochaetal disease, syphilis. Like syphilis, LD causes a wide range of (mostly) nonspecific symptoms and signs; there are 3 clinical stages: Stage I: Manifestations include fever, fatigue, headaches, myalgia, arthralgia (but not arthritis) and lymphadenopathy, usually within 2-3 weeks of infection. A characteristic skin lesion, erythema migrans (EM), appears 3-30 days after the bite of an infected tick, usually at the site of inoculation. The initial lesion is a red maculo-papular lesion greater than 5cm in diameter, rarely painful and expands and may reach more than 50cm in diameter, with central clearing and a well defined, circinate border ("bulls-eye"). Multiple lesions at different stages of evolution may be present. Allergic reactions, associated with tick bites, may be confused with early EM, but occur within a few hours of the bite and resolve within a few days. In North America, EM occurs in 60-80% of serologically confirmed cases of LD.

Stage II: Symptoms are non-specific and occur weeks or months after the tick bite. A causative association with LD is often uncertain. The lesions resemble those of secondary syphilis: carditis, chronic meningitis, mononeuritis (eg Bell's palsy) and conjunctivitis. Arthralgia and myalgia are often prominent.

Stage III: Symptoms occur months or years after exposure. The most typical feature, North American, is an erosive arthritis of large joints, particularly the knees. A chronic skin manifestation, acrodermatitis chronica atrophicans (ACA) occurs, mainly in European patients. Recently, four genospecies of B.burgdorferi have been described; B. burgdorferi sensu stricto, B. garinii, B. afzelii and B. japonica. They are associated with different patterns of disease, any of which can mimic other diseases. With the possible exceptions of typical EM and ACA associated with appropriate exposure, clinical features alone are insufficient for diagnosis of LD and laboratory tests are required for confirmation.

Diagnosis Culture/PCR Isolation of the causative organism from a punch biopsy taken at the edge of the EM lesion is successful in up to 80% of cases but it may be up to 8 weeks before spirochaetes can be detected. Polymerase chain reaction (PCR) has the advantage of greater sensitivity and speed; a result is available within 24 hours. Isolation and/or PCR should be attempted upon presentation of a patient with an EM lesion. Serology Laboratory diagnosis of late LD (Stage II & III) is less reliable and depends on serological tests including the indirect fluorescence antibody test (IFAT), enzyme linked immunosorbent assay (ELISA) and Western immunoblot (WB). False positive results occur due to cross reactions with other bacteria, especially other spirochaetes, viruses and in unrelated syndromes such as autoimmune diseases. IFAT and ELISA are used as screening tests but there has been little standardisation of methods. Any borderline or positive results should be confirmed by WB which can detect protein bands specific for B. burgdorferi. However, nonspecific bands occur, particularly with the highly cross reactive 41kDa (flagellin) protein. At the Sixth International Congress on Lyme Borreliosis a standardised interpretation of WB results was accepted: an IgG immunoblot is considered positive if 5 of the following 10 bands are present: 18, 21, 28, 30, 39, 41, 45, 58, 66 and 93kDa. Patients with late stage LD will show 10 or more bands on a WB.

Treatment The antibiotic therapy of early LD generally results in complete recovery. A 2 week course of oral doxycycline or amoxycillin for Stage I and a third generation cephalosporin for Stage II are the most commonly used regimens. Treatment of late stage LD is less successful and a chronic or relapsing course is common. A third generation cephalosporin for 3 weeks is recommended.

Prevention The prevention of LD is mainly through avoidance of tick infested areas and of tick bites by the use of repellents (particularly those containing DEET), wearing of light coloured clothing so that ticks are more easily seen and prompt removal of attached ticks. Transmission of spirochaetes generally does not occur until after 24 hours attachment of the tick. Antibiotic prophylaxis is not recommended. Trials of LD vaccines are in progress with varying degrees of success.

LYME DISEASE IN AUSTRALIA History - Australia The first Australian cases of a syndrome consistent with Lyme disease were reported from the Hunter Valley region of New South Wales in 1982. Serology was initially negative on one of the 6 patients, but later reported as positive in low titre. Cases of EM with febrile illness were reported in 1986 from the south and central coasts of New South Wales. All had negative serology. In Queensland, from 1986 to 1989, the State Health Laboratories tested 1,247 patients for B.burgdorferi antibody using an IFAT and reported 186 (15%) positive (titre 64) titres. In none of these cases was confirmatory serology (WB) undertaken. In 1988 at Westmead Hospital, a multidisciplinary investigation of putative LD in coastal New South Wales began, encompassing clinical, serological, vector and reservoir host studies.

Clinical investigations - Australia Over the past 6 years, due principally to local publicity, there has been an increase in serological testing for LD. This is often initiated by patients, who believe that LD may be an explanation for an undiagnosed health problem. Thus, most patients seen by infectious diseases specialists are self selected and referred for assessment on the basis of tick exposure and reported positive screening serology. Patients frequently have long-standing symptoms for which no other diagnosis has been established including myalgia, arthralgia without objective evidence of joint disease, neurological symptoms such as frequent headaches, inability to concentrate and impairment of memory, and syndromes resembling chronic fatigue syndrome. The late LD dermatological manifestation, ACA, has not been reported in Australia. A few cases of EM have been reported from South-Eastern Australia. However, diagnosis can be confounded by a spectacular erythematous hypersensitivity reaction to the bite of I. holocyclus, the most common tick biting humans in New South Wales. Of eight skin biopsies submitted to Westmead Hospital for spirochaete isolation, one, from a patient returning from a LD endemic area in Europe, was culture positive for B.burgdorferi. There has been no isolation from local patients. Serological Investigations - Australia No significant difference was found in seroprevalence rates for B.burgdorferi infection in humans between high (rural residents) and low (urban residents) tick exposure groups, using an IgG ELISA. The overall seropositive rate was 2.2% (9/400). The seroprevalence in New South Wales is comparable with that in non-LD areas, where 1- 3% of human sera are seropositive due to cross reacting antibodies and contrasts with reports from known endemic areas, outside Australia, where rural populations have considerably higher seropositive rates. A serosurvey of dogs in New South Wales showed a similar result with 2.5% (6/239) seropositive and another from Brisbane also showed no evidence of B.burgdorferi infection. These suggest that southeastern Australia is a non-endemic area. From 1988 to 1994 at Westmead Hospital, 78 (1.8%) of 4,372 from local patients with suspected LD were positive for IgG by ELISA and IFAT. All 78 were tested by WB, using North American and European strains of Borrelia; 46 sera showed one or more bands. None, including those with putative late stage disease, showed more than 4 specific bands and thus were all negative by international criteria. Twenty-four patients with various bacterial, viral or autoimmune syndromes unrelated to LD were tested in parallel and 11/24 showed one or 2 indicative bands. Thus a high degree of cross reactivity was demonstrated with non-LD patients. Recently, there have been reports from eastern Australia of LD-like illness associated with WB serology yielding bands at 31kDa (OspA) and the highly-cross reactive 41kDa band. None of these results conforms with internationally accepted criteria for a positive WB. Concomitant with this are results of WB analysis of sera from patients with syndromes unrelated to LD, >30% of which reacted with a 41kDa band and >10% with the OspA band. The sensitivity of serological testing for LD sometimes depends on the strain of Borrelia used and could confound interpretation of results in Australia, where no local spirochaete has been isolated for use as a reference antigen. Vector and Reservoir Host Investigations - Australia To detect a possible causative agent, ticks were collected from areas associated with putative infections and examined for spirochaetes by dark field microscopy, culture of gut contents, and direct testing of ticks with PCR for the Borrelia-specific flagellin gene. In total, over 12,000 ticks were tested including >1,000 by PCR. Spirochaete-like objects (SLOs), were observed in 92 cultures from bloodfed ticks but were not typical of Borrelia spp. They were found only found in cultures with bacterial contaminants, presumably from the bloodmeal. Electron micrographs were similar to those of SLOs recovered from contaminated cultures from ticks in Missouri, USA and were composed of aggregations of bacterial flagella, thought to originate from the contaminants. Molecular characterisation indicated that the SLOs shared some antigens with B.burgdorferi, but were not genetically related. Similar objects found in cultures from dissected bloodfed ticks taken from animals on the mid-north coast of NSW were purported to be related to B.burgdorferi and the probable cause of LD in Australia. A small number (17) of native vertebrate animals were sampled by ear punch biopsy for culture and PCR investigation but there was no evidence of borreliae. It is possible that the PCR primers used were unable to identify Australian spirochaetes. However, the tick gut contents were also negative by culturing and dark field microscopy.

Conclusions - Australia There are some major differences between Australia and the endemic areas of the northern hemisphere with respect to the natural history of LD: No ticks of the I. persulcatus complex, the principal vectors to humans in the northern hemisphere, occur in Australia. In eastern Australia, the logical candidate vector would beI. holocyclus which has a wide host range and is the most common tick biting humans. It was unable to transmit a North American strain of B.burgdorferi but an association with a so far undiscovered Australian spirochaete can not be excluded. None of the mammal species identified as reservoir hosts in the northern hemisphere are present in Australia. There are reports of spirochaetes in Australian native animals, and a local mammal could be a reservoir host for an indigenous spirochaete that occasionally infects humans through a tick vector and produces a clinical syndrome similar to LD; however, no spirochaete was detected in the 12,000 ticks or animals processed.

Summary The diagnosis of LD outside known endemic areas cannot be based solely on serological tests especially if they fail to conform with internationally accepted criteria, because of the high incidence of false positive results. A clinical diagnosis in a non-endemic disease area (especially of Stage II or III disease), is difficult to support without isolation of the causative agent from the patient, from other patients with similar illness or from a known vector in the region. The existence of LD in Australia will remain controversial until an organism is isolated from a local patient and fully characterised, or until a tick-borne organism can be shown to be responsible for the human infection. If it exists it shares few of the epidemiological or clinical characteristics of US or European patterns of LD. Further Reading Baldock, F.C., Yamane, I., and Gardner, I. (1993). Pilot survey for Lyme disease antibodies in Brisbane dogs. Australian Veterinary Journal, 70:356-7. Barbour, A.G. and Fish, D. (1993). The biological and social phenomenon of Lyme disease. Science, 260: 1610-1616. Dickeson, D. and Gilbert, G.L. (1994). Lyme Disease in Australia? Western immunoblots not the final answer. Annual Scientific Meeting Australian Society of Microbiology, A125. DOGGETT, S.L., RUSSELL, R.C., Munro, R., Dickeson, D., Ellis, J. Avery, D., Hunt, C.L., Simmonds, J. and Trivett, N. (1994). Lyme disease - the search for the causative agent in southeastern Australia. Arbovirus Research in Australia. Arbovirus Research in Australia, 6: 313-315. Hudson, B.J., Barry, R.D., Shafren, D.R., Wills, M.C., Caves, S.F. and Lennox, V.A. (1994). Does Lyme borreliosis exist in Australia? Journal of Spirochaetal and Tick-Borne Disease; 1: 46-51. Piesman, J. and Stone B.F. (1991). Vector competence of the Australian paralysis tick, Ixodes holocyclus, for the Lyme disease spirochaete Borrelia burgdorferi. International Journal Parasitology, 21: 109-11. RUSSELL, R.C., DOGGETT, S.L., Munro, R., Ellis, J., Avery, D., Hunt, C., and Dickeson, D. (1994). Lyme disease: A search for a causative agent in ticks in southeastern Australia. Epidemiology and Infection, 112: 375-384. RUSSELL, R.C. (1995). ?Lyme disease in Australia - still to be proven! Emerging Infectious Diseases, 1: 29-31. Wills, M.C. and Barry, R.D. (1991). Detecting the cause of Lyme disease in Australia [letter]. Medical Journal of Australia, 155: 275.

Stephen L. Doggett, Richard C. Russell, Richard Lawrence and David Dickeson Originally appeared in: Inoculum, 4: 1-4. Modified and updated; November, 1997. Related Links (Information from America for ticks, Lyme disease, Ehrlichiosis, Human Babesiosis). (Lyme disease from Europe, tick biology, control and images). (Lyme disease network from America).

Malaria Overview Natural History Symptoms Mosquito Vectors Epidemiology Prevention Malaria in Australia

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Overview This disease in humans results from infection with a protozoan blood parasite transmitted by a species of the mosquito genus Anopheles. The human clinical condition known as malaria is caused by infection with one of four species of the genus Plasmodium: Plasmodium falciparum, P. vivax, P. malariae, and P. ovale. The first two are the most common and most important, and P. falciparum infection often can be fatal in the absence of treatment.

Natural History The Plasmodium species are blood parasites, although some also invade liver cells where they lie dormant until later release brings a relapse with fevers associated with the destruction of red blood cells. The vector mosquitoes imbibe the parasites with the bloodmeal, and the sexual stages unite in the mosquito gut to create a stage which invades the gut wall and forms a cyst, which in turn releases many infective stages (sporozoites) which invade the salivary glands, and are injected into a new host when the mosquito feeds. The sporozoites invade liver cells and later developmental stages of the parasite invade red blood cells which they disrupt (causing fever), form sexual stages and the cycle is completed.

Symptoms Malaria is characterised clinically by fever (usually periodic), varying degrees of anaemia and splenic enlargement, and a range of syndromes resulting from the physiological and pathological involvement of certain organs, including the brain, liver and the kidneys.

Mosquito Vectors Mosquito vectors of human malaria vary with global region and sometimes even locality, but all belong to the genus Anopheles. However, not all Anopheles can transmit the parasites; relatively few species are important primary vectors, with others of secondary importance, and many of little or no consequence.

Epidemiology Malaria is one of the most widespread of all human parasitic diseases, and in the early part of the last half century more than two-thirds of the world's population lived in endemic areas. By about 1950 it was estimated that the annual incidence of the disease was approximately 250 million cases, with about 2.5 million deaths per year, and significant interference in the agricultural and industrial development of tropical countries. From the 1950s, the World Health Organisation instigated and co-ordinated efforts towards worldwide eradication of the disease. By the early 1970's the population freed from the risk of malaria transmission had increased from 400 million to over 1200 million, with the disease being eradicated from the whole of Europe, most of North America, most of the Caribbean and large parts of South America, and Singapore, Japan, Korea, Taiwan and Australia. However in recent years the position has deteriorated in some countries where control efforts were making an impact, and the disease has returned to others from which it had been regarded as eradicated. In Africa south of the Sahara, where little eradication has been attempted, the distribution of malaria has remained essentially unchanged. In 1988, the global incidence of malaria was estimated to be of the order of 110 million cases annually with some 270 million people infected. At the present time, the momentum for global malaria eradication has declined, and few tropical countries maintain the enthusiastic and often efficient vector control efforts that existed in the 1960's.

Prevention Prevention of malaria in many countries has been heavily dependent on anti- malarial drugs and residual insecticides since the 1950s, but this has broken down in a lot of places for various reasons, including development of drug resistance by the parasites, insecticide resistance by the mosquitoes, and failures in administrative and logistical systems at central, regional and local government levels. Thus, the importance of self protection for local inhabitants and visiting travellers in "at-risk" areas has become more and more emphasised in recent years. This involves the use of protective clothing where possible, use of chemical repellents, and the use of bed nets when sleeping in unscreened or otherwise unprotected situations. Drugs for protection against infection are still useful in certain areas, but expert advice should be sought with respect to the regions and localities being visited, the time to be spent there, and other factors likely to relate to exposure to infection.

Malaria in Australia In Australia, malaria has been endemic, but the malaria was declared eradicated from the country in 1981. Little is known of local vectors because few outbreaks were studied. However, laboratory investigations have revealed that a number of local Anopheles species are susceptible to infection, and An. amictus, An. annulipes, An. bancroftii, An. farauti and An. hilli have been possibly involved in field transmission. Anopheles farauti is a major vector of malaria in Papua New Guinea, and it is presumed to be the species of greatest concern in the north of Australia. However, this ‘species’ is recognised to be a complex of closely related species, the members of which cannot be differentiated by eye, and the capability to transmit malaria of the different members is unknown. In southern Australia, An. annulipes has apparently been the vector where occasional cases of malaria have been contracted, but this ‘species’ is likewise a species complex and the relative capacities of the various members to transmit malaria is also unknown. Although malaria is no longer endemic in Australia, approx. 700-800 cases occur here each year in travellers infected elsewhere, and the region of northern Australia above 19oS latitude is the receptive zone for malaria transmission. Occasional cases of local transmission occur in the Torres Strait islands and rarely in northern Queensland, and vigilance is required to prevent reestablishment of the infection in some northern localities.

Mosquitoes

 Natural History  Mosquito borne diseases  Clinical Presentation  Laboratory Diagnosis  Treatment and Control  Confirmation and Enquiries  Links

modified from: Kettle, D.S. (1995). Medical and Veterinary Entomology. CAB International. Wallingford

bottom of page Natural History Mosquitoes are blood sucking insects that are responsible for the transmission of many diseases throughout the human and animal populations of the world. Within Australia there are more than 300 different species of mosquito but only a small number are of major concern. Several important human diseases are transmitted throughout Australia by these insects including Dengue fever, Australian encephalitis, Ross River virus disease and Barmah Forerst virus disease; malaria has been transmitted locally in Australia only rarely in recent decades. In addition to being disease vectors, mosquitoes can cause major disruptions, through their persistent biting, to occupational, recreational and social activities. Mosquitoes belong to the family of flies called Culicidae and are small fragile insects modified from: Goddard, J. (1993). A Physician's Guide to Arthropods of Medical Importance. CRC Press. Florida. that have six delicate legs and two wings covered in scales. The head of a mosquito is equipped with a projecting proboscis which conceals and protects the long piercing and sucking mouthparts. These biting insects have a complex life cycle; the immature stage is totally aquatic and the adult is terrestrial. The adult female returns to a water habitat for a brief period to lay each batch of eggs. Mosquito species vary in their breeding habits, biting behaviour, host preferences and flight range. Most mosquitoes disperse less than two kilometres; some move only a few metres away from their original breeding place, others can fly some 5 or 10 kilometres, and a few species will disperse up to 50 kilometres downwind from the larval habitats. On average, a female mosquito will live 2-3 weeks, but the male's lifespan is shorter. Within their lifetime both adult male and female will feed on nectar and plant fluids, but it is only the female that will seek a blood meal. The majority of species require this blood meal as a protein source for egg development. Female mosquitoes are attracted to a potential host through a combination of different stimuli that emanate from the host. The stimuli can include carbon dioxide, body odours, air movement or heat. Upon locating a suitable host, the female will probe the skin for a blood capillary then inject a small amount of saliva containing chemicals which prevent the host's blood from clotting. This is often the pathway for potential pathogens such as viruses to enter a host. After engorging on the host's blood the female will find a resting place to digest her meal and develop eggs before flyingoff to deposit them in a suitable aquatic habitat. On hatching, the young larvae (wrigglers) feed continuously and grow through four different instars or moults. Larval development is dependent on the availability of food and prevailing conditions, particularly temperature, but generally takes at least one to two weeks. The final larval instar develops into an active comma- shaped pupa (tumbler) from which the adult mosquito emerges about 2 days later to feed, mate and develop eggs for the next generation.

Mosquito-borne diseases in Australia Diseases transmitted by mosquitoes in Australia include Dengue fever, Australian encephalitis, Ross River virus disease and Barmah Forerst virus disease. Dengue is the most important viral disease transmitted by mosquitoes afflicting humans in a world context. Clinical symptoms range from mild fevers, to a severe and potentially life threatening haemorrhagic disease. In Australia, Dengue fever is restricted to Quensland where the major vector Aedes aegypti occurs. "Australian encephalitis" (AE), or "Murray Valley encephalitis" are synonyms for a clinical syndrome caused by infection with Murray Valley encephalitis virus or Kunjin virus. Symptoms are variable, from mild to severe with permanent impaired neurological functions, to sometimes fatal. Cases of AE occur sporadically in northern Australia and especially in the northwest of WA, but there have been no cases of MVE recorded in southeastern Australia since 1974. Ross River (RR) and Barmah Forest (BF) disease have been collectively known as "Epidemic Polyarthritis", however the two diseases have a slightly different clinical picture. A wide variety of symptoms may occur from rashes with fevers, to arthritis that can last from months to years with RR virus infection. RR disease is the most commonly reported mosquito transmitted disease to humans (over 6,500 cases in 1997) and occurs in all states of Australia. There are occassional local epidemics with hundreds to thousands of infections, with many going unreported. BF disease occurs in most states of Australia, although the annual number of cases are around 1/10th that of RR disease. A series of outbreaks during the early 1990's has highlighted the increasing importance of BF disease. Malaria in Australia has been endemic, but was declared eradicated from the country in 1981. However, approximately 700-800 cases are imported annually from travellers infected elsewhere.

Clinical Presentation Sensitivity to mosquito bites varies with individuals, most people have only a mild reaction but others can have severe symptoms from the saliva of mosquitoes. Typical symptoms include swelling, redness and irritation at the puncture site. If the bites are scratched or traumatized, they may become infected with bacteria and a secondary infection can be initiated, especially on the lower limbs. The diagnosis of mosquito- borne diseases including Dengue, Australian encephalitis, and Ross River and Barmah Forest viruses can only be confirmed with appropriate blood tests.

Laboratory Diagnosis Mosquitoes are identified with the aid of a stereo microscope and taxonomic keys. The detection of viruses and other pathogens in mosquitoes is undertaken. Detection of viruses or virus antibodies in human blood is a procedure performed in the arboviral serology unit at Westmead Hospital.

Treatment and Control There are many methods of control that can be implemented to reduce the number of mosquitoes. Local councils may use larvicides (pesticides that kill the larvae) which prevent mosquitoes from maturing to adults. In areas where there is a disease outbreak fogging may be considered as an option in order to kill the infected adult mosquito population. Other methods could include the use of parasites, predators or pathogens of mosquitoes to assist in reducing the population, but there is no biological control agent other than fish currently available for use against mosquitoes. Simple measures can be taken by individuals to limit their contact with mosquitoes, Areas that are known to be infested with large numbers of mosquitoes shold be avoided. Activities that are scheduled for outdoors, especially around dusk should be limited, as the biting activity of many mosquitoes will peak during this period. Clothing that has long sleeves and long pants should be worn when visiting areas that are infested with mosquitoes. A chemical repellent that contains approx 20% DEET (diethyl toluamide) should be used on exposed areas of skin, but not repeatedly on young children. Windows and doors should be screened; water tanks also, using a small gauge mesh to exclude mosquitoes from these potential breeding sites. Empty all containers throughout the garden that hold water such as pot plant saucers, tyres, roof guttering and tins to prevent breeding. Bed nets are an effective barrier against biting insects at home or camping, and can now treated safely with an insecticide. Insecticidal sprays, and coils and electric mats, for use around the house can help in keeping mosquitoes at bay.

Confirmation and Enquiries Identification of mosquitoes and all other medically important arthropods is preformed through the Medical Entomology Department at ICPMR, Westmead Hospital. See 'Contacts' for further information.

Related Links (University of South Australia mosquito research group). (Comprehensive list of mosquito related sites from the United States). (A review of mosquito seeking behaviour). (Mosquito Genomics server). (American mosquito control association). (Links to mosquito sites in America).

Murray Valley Encephalitis virus & Kunjin virus

Overview Natural History Symptoms Laboratory Diagnosis Treatment Prevention Further Reading

bottom of page Overview ‘Australian encephalitis’, or ‘Murray Valley encephalitis’ are synonyms for a clinical syndrome caused by infection with Murray Valley encephalitis (MVE) virus or Kunjin (KUN) virus. Symptoms are variable, from mild to severe with permanent impaired neurological functions, to sometimes fatal. Mosquito avoidance measures are the best form of prevention.

Natural History The term 'Australian encephalitis' (AE) has been used to indicate encephalitis induced by infection with either Murray Valley encephalitis (MVE) and/or Kunjin (KUN) virus. However, they are different viruses, with slightly different clinical symptoms and so the infections should be named after the causative virus (i.e. MVE disease/KUN disease). The first reports of disease that might be attributed to MVE infection in humans in Australia occurred in southeastern Australia in 1917, 1918 and 1925 (114, 67 and 10 cases respectively), and were described under the title of "Australian 'X' disease". A virus, designated Murray Valley encephalitis virus, was later isolated from fatal cases in an epidemic in 1951, when there were 48 cases (and 19 deaths), and this virus has been accepted as the causal agent of the earlier Australian 'X' disease outbreaks. The next major outbreak occurred in 1974; although 42 cases were recorded in the southeast (primarily in the Murray Valley region), human infections occurred in all mainland states, with a national total of 58 cases and 13 fatalities. Serological studies indicated that some non-fatal cases were due to KUN virus infection, although only MVE virus was associated with fatal cases. Since 1974, cases have occurred sporadically in northern Australia and in the northwest of WA in particular, but there have been no cases of MVE recorded in southeastern Australia. However, in 1984 there was a case of non-fatal KUN encephalitis in northeastern Victoria and KUN infections were reported from two other areas in the Murray Valley, and in 1991 there were two KUN infections reported in southwestern NSW. It is now generally acknowledged that both MVE and KUN viruses have a natural endemic cycle, which involves water birds as the vertebrate host and Culex annulirostris (which breeds in freshwater environments) as the major vector, in northern regions of Australia. The proposal that the virus is endemic in northern Australia is supported by serological studies in Queensland and in northern Western Australia. MVE virus activity has been shown to be continuous in the Kimberley region of Western Australia, and it appears that foci of MVE and KUN exist at least in northern Western Australia, and possibly in the NT and northern QLD. Epidemic activity in the southeast has been associated with excessive rainfall which increases bird and mosquito populations and leads to a virus overflow infecting humans. It is still uncertain whether the virus/es are introduced to the southeast prior to outbreaks, or whether they are endemic there at undetectable levels and only become evident with periods of intense bird and mosquito breeding following extensive flooding. Certainly, there is an association of previous outbreaks in the southeast with extraordinary rainfall and widespread flooding in the eastern Australian watersheds and the Murray-Darling basin in particular.

Symptoms For MVE virus infection, there is a high subclinical rate and perhaps only 1 in 500 or more infections becomes noticeably ill. Cases vary from the mild to severe and fatal. Symptoms almost invariably include a sudden onset of fever; anorexia and headache are common, while vomiting, nausea, diarrhoea and dizziness may also be experienced. Brain dysfunction may be experienced after a few days with lethargy, irritability, drowsiness, confusion, convulsions and fits; neck stiffness can be expected, and both coma and death may ensue. It is rare for recovery from the encephalitic syndrome to occur without some residual mental or functional disability.

Laboratory Diagnosis A variety of blood tests are used to demonstrate the presence of specific antibodies to MVE and KUN virus. Blood samples should be taken during the acute and convalescent phases of the illness, and a fourfold rise in antibody levels will confirm the clinical diagnosis.

Treatment As there are no specific therapies to treat the disease or control the virus, supportive treatments are used (such as respiratory support in severe disease).

Prevention Prevention of mosquito borne viral diseases is mainly accomplished through reducing the threat of bites from mosquitoes. This can be achieved either through undertaking active mosquito control or by the use of personal protective measures. A variety of active mosquito control measures are available including habitat modification in order to reduce water availability for breeding of the larval stage, through to the use of appropriate insecticides to control both the larval and adult mosquito stages. These are large scale control measures which can only be undertaken by government bodies, generally local councils. Personal protective measures include: avoiding known mosquito infested areas, especially at dawn and dusk when mosquitoes are most active; ensuring that houses are adequately screened; using insect repellents that contain the chemical DEET, and reapplying it regularly; wearing long sleeved shirts and pants. Other preventative measures include government based programs that undertake mosquito monitoring and virus surveillance from mosquitoes. These programs aim to act as an early warning system for virus activity by monitoring mosquito populations, viruses such as MVE or KUN and weather patterns. In New South Wales, such a program has been running for several years at the Department of Medical Entomology at Westmead Hospital and is funded by the NSW Health Department.

Further Reading Boughton, C.R. (1996). Australian Arboviruses of Medical Importance. Royal Australian College of General Practitioners, Melbourne, pp 67. RUSSELL, R.C. (1995). Arboviruses and their vectors in Australia: an update on the ecology and epidemiology of some mosquito-borne arboviruses. Review of Medical and Veterinary Entomology, 83: 141-158. RUSSELL, R.C. (1993). Mosquitoes and Mosquito-Borne Disease in Southeastern Australia. Revised edition. Published by the Department of Medical Entomology, Westmead Hospital. xii + 310pp. Marshall, I.D. (1988). Murray Valley and Kunjin Encephalitis. in Monath, T. (ed). The Arboviruses: Epidemiology and Ecology, Volume III. CRC Press, Florida, pg: 151-190. Non-Biting Flies

 Natural History  Clinical Presentation  Laboratory Diagnosis  Treatment and Control  Confirmation and Enquiries

modified from: Kettle, D.S. (1995). Medical and Veterinary Entomology. CAB International. Wallingford

bottom of page Natural History Non-biting flies have developed a close relationship with human habitation over many centuries which has basically benefited the fly populations. This association has resulted in the deaths of thousands of people, due to the ability of this humble insect to transmit disease. Non-biting flies have adapted to the different niches available within a human population which permit them to feed, grow and reproduce. Their feeding and breeding habits enable these commensal flies to be effective mechanical vectors of disease to humans. The life cycles of flies are complex, but each species has the same developmental stages in common, consisting of an egg, larval (maggot) stage, pupa, and finally the adult. Growth at each immature stage is dependent on many variables but primarily temperature and suitable substrates for a food supply. Each adult fly has its own special requirements that must be met before mating and egg laying (oviposition) commences. Non-biting Australian flies contain many species that are of medical significance. These flies are responsible for contamination and spoilage of foodstuffs, annoyance, mechanical transmission of disease-causing pathogens, and invasion of living tissues (myiasis). Collectively known as "filth flies", they are distributed throughout the families of Calliphoridae (blow flies), Sarcophagidae (flesh flies) and Muscidae (house flies). Non-biting flies are often associated with domestic dwellings, especially throughout the warmer months when flies bred prolifically, invading homes and can be a constant annoyance for humans. Flies are equipped with special sensory cells on their antennae and feet which enable them to locate suitable food and egg laying sites. These sensory cells aid in detecting compounds such as ammonia, carbon dioxide and other strong compounds that are emitted from decomposing organic materials, such as carrion and faeces. The free interchange flies have with such sites ensures the flies are laden with bacteria on their mouthparts, body hairs and the sticky pads of their feet, as well as in their stomachs (where the bacteria rapidly multiply), faeces and vomitus. Contact with any foodstuffs, or feeding, which often involves vomiting and defecating, will contaminate food, preparation surfaces and utensils with potentially disease causing organisms. Eggs or young larvae may also be deposited if the substrate is deemed suitable for oviposition by the fly. Flies can be strongly attracted to uncovered, malodorous wounds, body openings, open sores or damaged skin. Some species will deposit their eggs or larvae on the site if the circumstances are suitable. This can result in myiasis, wherein young maggots feed on healthy or diseased tissue to complete their growth cycle. Some species of fly are well known for their nuisance value, such as the "bush fly", Musca vetustissima. This fly is a major pest which breeds in manure in pastures and disperses widely to surrounding rural and adjoining urban environments throughout the summer months. These flies are annoying, constant companions of humans and livestock which they visit in large numbers, and attempt to feed at the mouth, nose, eyes or wounds at every possible moment. Bushflies have been known to transmit eye infections and other enteric diseases by their continual interchange between other animals and humans. Another two species that can be bothersome are the "common house fly", Musca domestica and the "lesser house fly", Fanniacanicularis. Recent research overseas has revived the interest in the "benefits" of some maggots and some medical units are now using "clean" maggots to aid in the cleansing of decaying flesh of humans. This supervised introduction of maggots to otherwise slow healing wounds can be beneficial in promoting healing and can lead to a enhanced recovery of the affected tissue. The science of forensic entomology has also recognised maggots as a useful tool as an aid in determining the time of death in humans. Flies are the first insect to locate and oviposition on a corpse, in fact some species arrive within minutes of death, but various species arrive at different stages of decomposition; identification and ageing of the resulting maggot population in a body can lead to an estimation of the "time since death", and this can be beneficial in murder investigations. Returning tourists or overseas visitors to Australia from countries in Central and South America, and Africa can unknowingly bring with them the immature stages of certain flies. From Central and South American countries the human bot fly, Dermatobia hominis, is a frequent souvenir. African countries provide other species including Cordylobia anthropophaga (the Tumbu fly) and Cordylobia rodhaini (Lund's Fly). Each of these species of fly has a perculiar and interesting life history that brings them in close contact with humans or livestock producing a furuncular (boil-like) myiasis. When skin contact is made, usually with normal healthy tissue, the young larvae immediately burrow into the skin and develop through a further two molts, before emerging to pupate in the soil and mature to the adult. Over this growth period of several weeks the lesions grow to large, painful boil-like structures which house the growing maggot. Efficient air travel has made the transportation of these larvae to other continents very easy and often rapid. People can be in another part of the world before the larvae have completed their life cycle, which makes accidental introduction of an exotic species of fly to other countries a constant threat to livestock and human habitation (see the Myiasis Flies Fact Sheet for more information).

Clinical Presentation Patients exhibit a vast number of symptoms in relation to fly problems. Disease-causing organisms that have been isolated from flies include enteric pathogens such as Salmonella and Shigella and typhoid bacteria (food poisoning), plus various parasites such as pinworm and tapeworm; however, in modern developed societies with high standards of hygiene, fly-borne disease is relatively uncommon. With respect to the flies that affect patients with pain and discomfort associated with myiasis, some of the larger exotic species can produce painful boil-like swellings or simply a disgusting appearance on a wound. Removal of these maggots may simply require irrigation of the wound and subsequent antibiotic treatment as necessary, or with subctuaneous infestations a forced expulsion of the maggot by cutting off it's air supply with petroleum jelly; however, sometimes surgical intervention may be necessary. Other species of maggots are often recovered from patients' faecal material or urine, or associated clothing, indicating oviposition has occurred in the genito-anal area; no fly has a development cycle involving ingestion by humans, so such instances should be seen as accidental or incidental contaminations. The isolation of maggots from vomit can usually be traced to spoilage of foodstuffs that were contaminated prior to eating.

Laboratory Diagnosis Flies are identified with the aid of a stereo microscope and taxonomic keys. Rearing of maggots to adult flies is often required for accurate identification.

Treatment and Control Properly fitting screen doors and windows are essential to exclude flies from homes and other areas where food is prepared. UV insect lights and air curtains used in industrial applications are effective but maybe cost prohibitive in a domestic situation. A combination of good sanitation and mechanical exclusion will produce the same effect and keep fly populations under control. Elimination of potential breeding sites will help in the general reduction of fly numbers. Pet faeces should be removed and fresh manure and other compost dug into garden beds. Routine emptying and cleaning of all garbage receptacles will reduce breeding. People travelling to destinations that may include rural areas of Africa, and Central and South America, should be aware of possible infection by the immature stages of several exotic flies.

Confirmation and Enquiries Identification of non-biting flies, and other medically important insects, is performed through the Medical Entomology Department at ICPMR, Westmead Hospital.

Pubic Lice  Natural History  Clinical Presentation  Laboratory Diagnosis  Treatment and Control  Confirmation and Enquiries

modified from: Service, M.W. (1980). A guide to Medical Entomology. Macmillan. London.

bottom of page Natural History Pubic lice, or Pthirus pubis, are commonly referred to as crab lice or simply ‘crabs’. This name has come from the crab-like appearance and slower movement compared to other lice, such as the head louse, Pediculus capitis and the body louse, Pediculus humanus that can infest humans. Pubic lice are found worldwide, they are haematophagous (feeds on blood), and strictly host specific to humans. Typically, they infest the hair of the pubic and perianal regions but are occasionally found in other areas where the hair is sparse and coarse. This includes the hair of the beard, moustache, eyelashes, armpits, and sometimes the chest and abdomen. The hair on the scalp is usually unsuitable, because of its fine texture closeness of the shafts, but pubic lice are occasionally found at margins of the head on the hairline. If children are infested, the lice will generally be found only in the eyebrows or eyelashes. The pubic louse is grey in colour, and smaller (1.25 -2.00mm) than the head and body louse. Their body shape is oval and broader than long, with four distinct lobe-like protuberances on each side of their abdomen. The lice have a small head with short antennae and simple eyes. Each of the six legs of the louse terminates in a claw, but claws on the second and third pair of legs are huge compared to the first pair which are slender. Within each claw there is an associated thumb-like projection which enables the louse to grasp body hair, securing them whilst they feed on blood using their mouthparts which are especially adapted for piercing and sucking. The lice blood feed intermittently over several hours. Adults and the three smaller nymphal stages usually remain and feed in a settled position. Pubic (and other lice) lice cannot burrow into the skin and do not live under the skin. The life span of adult lice is less than a month. A mature female louse will lay a total of 30 eggs (nits), laying up to 3 eggs a day. The eggs are smaller than the eggs of the other human lice, and are a darkish-brown with an opalescent sheen. Each egg is cemented to the shaft of coarse hair, and at skin temperature will hatch within 6-8 days. If the lice are forced off the host they will die within 24-48 hours. Pubic lice cannot infest the rooms or carpets of an infected person. Pubic lice are usually transmitted by sexual contact, and although this is the most common method, it is incorrect to assume this is the only means of transmission. Shared bath-towels and clothing, discarded clothing hanging in overcrowded locker rooms, children sleeping with an infected parent, or bedding that has recently been vacated by an infected individual can lead to infestations. Pubic louse infestations cannot be transmitted from animals. No known disease causing organism has been transmitted by pubic lice in Australia.

Clinical Presentation At each puncture site a red papule develops and the immediate area swells. Intense itching is common due to the host’s reaction to the foreign proteins in the saliva of the louse. If the infestation is left untreated, the infected individual can become sensitised. Continual scratching may lead to secondary infections, and in some cases swollen lymph glands, due to bacterial infection. If the infestation involves the eyelashes, and left untreated, the eyelids can become swollen and inflamed. With the majority of infestations, after the pubic lice have fed, a characteristic grey-blue or slate colouration appears at the feeding site, which may last for days. The coloured area can be 0.2-3.0cm in diameter, and may have an irregular outline deep in the surrounding tissues, although this does not always occur for each infestation of pubic lice, it is more characteristic of pubic than for body lice. This discolouration is thought to be a result of altered human blood pigments or a reaction to substances excreted from the louse’s saliva.

Laboratory Diagnosis Identification of louse specimens is by light microscopy.

Treatment & Control When pubic lice have been identified as the source of the problem, it is important that all sexual contacts of that person be made aware of the situation and treated if necessary. If one person within a family has pubic lice, all family members should be examined and treated, especially if the infected person shares a bed with other family members. Treatments for pubic lice are similar to those for head lice, and can be purchased from any pharmacy without a prescription. For eyelash and eyebrow infestations, an application of petroleum jelly twice a day for 7-10 days can be effective in controlling the lice. Careful mechanical removal of eggs will be required, as the lice apply cement like substances when gluing the eggs to the hair and they are difficult to remove. The infected person’s underwear and bed linen should be washed in hot water, followed by hot tumble drying to ensure all lice have been killed. Spraying rooms or beds with insecticides is unnecessary, as the lice can only survive for a limited time without a host.

Scabies

 Natural History  Clinical Presentation  Laboratory Diagnosis  Treatment and Control  Confirmation and Enquiries

modified from: Kettle, D.S. (1995). Medical and Veterinary Entomology. CAB International. Wallingford

bottom of page Natural History Sarcoptes scabiei is a parasitic mite that lives within the subcutaneous tissues of skin on humans, causing the condition known as scabies; similar mites cause what is called "mange" in wild and domestic animals. This mite is distributed worldwide, and can affect all socioeconomic groups. Scabies mites are generally host specific and S. scabiei is dependant on humans for its life cycle. These oval, straw coloured mites are very small, measuring 0.2-0.4mm in length. Their bodies are covered with fine lines and several long hairs. The female mite has scattered on the dorsal surface some short blunt spines, which aid her in maintaining her position within the tunnel. The mites have no eyes, and they have short and thick legs, with the first two pair of legs stalked. The immature stages of the scabies mite are comprised of a six legged larval stage, followed by 2 nymphal stages that have eight legs, and each stage resembles the adult mite. The entire life cycle of the mite occurs over 10-17 days. Newly mated females take approx. an hour to burrow into the outer layer of human skin and excavates a tunnel. The mite lays her eggs singly, depositing behind her 2-3 eggs each day. Females burrow without direction, using their mouthparts to tunnel 0.5-5mm a day, eating the skin and tissue fluids that ooze from their excavations. Each tunnel contains only one female, her eggs and faeces. After 48 hours the eggs hatch and the larval stages dig their way to the surface of the skin, where they immediately burrow. This burrow may only be a short distance into the skin, or they make use of hair follicles, to moult to the next stage. Larval and nymphal stages remain in these moulting pockets feeding on fluids secreted from the follicles before moulting to the adult stage. Newly moulted male and female mites construct short burrows <1mm before mating. After fertilisation, female mites wander on the skin to seek a suitable site for a permanent burrow, the transfer of a female to another host at this stage will initiate a new infection. A fertilised female mite can only initiate successful scabies infections. Female mites rarely leave their burrows, and if removed by scratching and remain undamaged, they will attempt to burrow again. During an infection the number of mites increases rapidly, then drops off, leaving infected persons with a relatively stable mite population of 15-20 females. The mortality rate of mites is high, 90% of mites that hatch will die, and mites removed from their host can only live a short time.

Clinical Presentation Scabies infestations can present different clinical pictures and may be difficult to diagnose. The initial infestation may remain undetected for a month or more, before sensitisation develops and a immunological response in the host is triggered. The allergic reaction is from components of the mite's faeces, skin moults, saliva or moulting fluids diffusing into the tissues of the host from the burrows. The patient can experience severe itching all over the body, and especially at night. Large areas of the body can be covered by a rash that can last for weeks but which will not (or only rarely) coincide with the areas of mite infestation. Eruption of the skin into small itchy lesions may occur in conjunction with the rash. Scabies mites tend to burrow into the skin where there is a natural crease and the host's reaction will be minimal. The hands, and webbing between the fingers, the wrists, and elbows are common areas. From the surface of the skin, the tunnels appear as greyish pencil marks, in darker skin the tunnels appear paler. The severe itching and scratching can lead to secondary infections and, in cases of heavy infestations anaemia can develop. There has been no transmission of disease pathogens associated with this mite. Untreated scabies infestations, especially in infants, immobilised geriatric patients, AIDS and other immunologically compromised patients can support huge numbers of female mites. The patient's skin may become crusted on the surface, with the underlying layers soft and honeycombed with tunnels, these infections are referred to as "Norwegian" or "crusted"scabies. Patients with this advanced state of infection can act as a source for local epidemics in health care facilities. In some cases, scabies infections in nursing staff or family that have had contact with the patient will lead to diagnosis of the primary patient. Reinfected patients will develop an immediate itch when another scabies infection is initiated.

Laboratory Diagnosis Skin scrapings are examined with a compound light microscope for the presence of mites, eggs or faeces. A glass slide mount is prepared, using dilute potassium hydroxide or lactic acid to mix with the skin scraping. This aids in clearing any thick layers of skin cells in the sample to reveal any evidence of the scabies mite, but clearing may take some time (hours to days).

Treatment & Control Once diagnosed, most scabies infections are easy to control, providing the directions of the scabicide treatments are followed. Any pharmacy will supply a chemical preparation, and a prescription is not necessary. Care should be taken in re-applying scabicides unnecessarily, to avoid skin irritation and added costs. In most cases, itching may persist for a week or more after the treatment, but this is not necessarily a sign of treatment failure. Re- examination of the patient at four weeks after the treatment is appropriate. At the commencement of the treatment, bed linen and underwear of the patient should be washed in hot water and hot tumble dried, but there is no need to treat furniture or rooms with an insecticide. A common problem of treatment failure is insufficient coverage of the body with the scabicide, and resistance is rare. For patients diagnosed with crusted scabies, the patient should be isolated, and barrier nursing implemented throughout the treatment. All individuals that have had significant contact with the primary patient should also be treated. Scabies is highly contagious in overcrowded situations and close contact with infected individuals should be avoided. Touching, shaking hands, or sharing beds and contaminated objects of an infected person are common modes of transmission.

Spotted Fevers

bottom of page In Australia, the Spotted Fevers are the main diseases transmitted by ticks to humans. There are two types of Spotted Fever, Queensland Tick Typhus (QTT) and Flinders Island Spotted Fever (FISF), although these diseases are not commonly reported (less than 50 cases of QTT per year in New South Wales). These afflictions are caused by rickettsiae (Rickettsia australisand R. honei, respectively), which are a group of primitive bacteria-like organisms. The symptoms of tick typhus include rashes, eschars, headaches, fever, flu-like symptoms and lymph node tenderness. The clinical diagnosis is confirmed through the use of specific blood tests. Tick typhus is treatable with antibiotics, although fatalities have occurred rarely. QTT is distributed along the eastern coastal strip of Australia from northern Queensland through northern New South Wales, at least as far south as Sydney, while FISF occurs in eastern Victoria and Tasmania (particularly in Flinders Island). It appears that the spotted fevers are transmitted to humans by the Paralysis tick, Ixodes holocyclus, but other species such as I. tasmani are also thought to be involved.

Ticks

 Introduction  Natural History  Clinical Presentation  Laboratory Diagnosis  Treatment and Control  Tick Removal

The female Paralysis tick,  Confirmation Ixodes holocyclus and Enquiries

bottom of page Introduction Ticks are bloodsucking, external parasites that are often encountered by people during activities in the Australian bush. There are many species known to attack humans and so samples should be referred to our expert laboratory for proper identification. Over the last twelve years, the Department of Medical Entomology, ICPMR has been at the forefront of research into ticks and tickborne disease, and has been the leading health authority for the provision of information on the ecology and control of this important public health pest.

Natural History The distribution of our most medically important tick, the Paralysis tick, Ixodes holocyclus, is roughly confined to a 20-kilometre band that follows the eastern coastline of Australia. As this is where much of the human population resides in NSW, encounters with these parasites are relatively common. Although most cases of tick bite are uneventful, some can result in life threatening illnesses including paralysis, tick typhus and severe allergic reactions. Ticks belong to the order Acarina, which also contains mites. The Australian tick fauna consists of approximately 75 species that can be divided into two families. The soft ticks (Family Argasidae) are represented by only a few species in Australia and are often associated with nests or resting places of animals. These ticks have a wrinkled appearance, which is akin to soft leather. The hard ticks, (Family Ixodidae), comprise the majority of our ticks and are distinguished by a hard dorsal plate in the shape of a fingernail and elongated mouthparts that have rows of backward pointing teeth. Some species of tick use these teeth in conjunction with a cement to remain attached to the host while blood feeding. The Paralysis tick can be found in a variety of habitats but are especially common in wet sclerophyll forests and temperate rainforests. They have very few predators, and are more likely to succumb to desiccation from high temperatures and low humidity. From the enormous numbers of eggs (2,500- 3,000) deposited in the moist leaf litter by the female before she dies, only a fraction of the eggs will survive and eventually grow to become adults. The six-legged larvae hatch after the eggs have incubated for 40-60 days. To moult to the next stage, the larval tick must obtain a blood meal. In searching for a host, they display a behaviour referred to as 'questing'; whereby the tick climbs to the top of nearest vegetation and waves its forelegs to and fro slowly, hopefully contacting a prospective passing host. This is usually a native animal such as a bandicoot, which is the main host, but also possums, kangaroos, and humans. This questing behaviour is undertaken each time a host is required for blood. Ticks usually do not climb more than around 50cm in the vegetation and there is no evidence to suggest that they fall out of trees. Once a suitable host is found, the larvae will blood feed for 4-6 days, drop from the host and moult to the eight-legged nymphal stage. Nymphs require a further blood meal for 4-8 days before moulting to the adult stage. Both female and male ticks quest for a host, but for different reasons; the female for a bloodmeal, the males to search the host for female ticks in order to mate and sometimes feed from them. Males may actually parasitise the female ticks by piercing their cuticle with their mouthparts to feed on her haemolymph (the tick's blood) and up to 3-4 males have been found feeding on one female tick. Male ticks rarely bloodfeed on a host. The adult female Paralysis tick will feed for up to around 10 days, drop off the host and lay eggs over several weeks. The entire life cycle of the Paralysis tick, involving 4 stages and 3 hosts, will take around a year to complete. Each life stage can be present throughout the year, although for the Paralysis tick, adults are more abundant in the spring and the early summer months, larvae in mid to late-summer, and nymphs during winter. Clinical Presentation Tick paralysis is most likely to be seen in children. The initial symptoms of tick paralysis may include unsteady gait, increased weakness of the limbs, multiple rashes, headache, fever, flu like symptoms, tenderness of lymph nodes, and partial facial paralysis. Tick paralysis develops slowly as the tick engorges, which will take several days. Despite the removal of the tick, the patient's condition typically will continue to deteriorate for a time and recovery is often slow. Undetected ticks are another possible reason for any prologed debilitation and should always remain a concern. Improvements in modern medicine and the development of a tick antitoxin have prevented further deaths from tick paralysis in the last 70 years. The antitoxin is available from the Commonwealth Serum Laboratories. Despite these developments, a few cases of tick paralysis in children are seen at major hospitals each year. Additionally, ticks take a high toll on pets every summer. Tick typhus is an infection with a rickettsia (bacteria-like organism) transmitted from native animals by ixodid ticks and is confined to the eastern coast line of Australia and Bass Strait Islands. Clinical symptoms include headaches, multiple rashes, swollen glands, fever and flu like symptoms. The disease is rarely fatal and is commonly treated with antibiotics. Lyme disease is a tick-borne infection common in the northern hemisphere and is caused by spirochaete bacteria. Symptoms are varied and may include rashes, fever, muscle and joint pain, and arthritis. The disease is not fatal and treatable with antibiotics. Despite clinical cases being reported from the early 1980's, there has been no confirmation that the disease occurs in Australia. (for more information go to the Fact Sheet on "Lyme Disease"). Allergic reactions are the most serious medical condition associated with ticks. These reactions can vary from a mild itching with localised swelling to widespread swelling with pain (click here to see one such reaction) to a severe and life threatening anaphylatic condition. Unlike with most other medical conditions associated with ticks, severe allergic reactions may occur with any tick stage. For people who develop severe allergic reactions, it is imperative that they must always avoid contact with ticks and avoid potential tick infested areas.

Laboratory Diagnosis All stages of ticks are identified with the aid of a stereomicroscope and taxonomic keys, but many species are difficult to identify accurately. The Department of Medical Entomology provides a specialist identification service.

Treatment and Control The best method of avoiding ticks is to stay away from known tick infested areas. If visiting such an area, light coloured clothing should be worn, as ticks will be much easier to detect. Trousers should be tucked into socks and shirts into pants. An insect repellent containing DEET or Picaridin should be applied, with a cream repellent applied to the skin and a spray repellent to footwear and clothing (note that DEET can damage some synthetic clothing). The repellent should be reapplied every few hours. All clothing should be removed on returning home and placed into a hot dryer for 20 minutes, which will kill any ticks that may still be on the clothing. Note that ticks can wander on the body for some two hours before attaching. This is how they become attached to the head (contrary to popular belief, they do not fall out of trees). The body should thereafter be searched well for ticks, especially behind the ears and on the back of the head. Children and pets should be examined for ticks after visiting bushland areas. In locations where people live where they contact ticks in their backyard, then strategies can be undertaken to reduce the tick population and thereby minimise exposure. The Paralysis tick is very susceptible to dry conditions and so decreasing soil moisture can lessen their impact. This can be achieve through the reduction of foliage cover, which increases sunlight penetration to the ground, reducing the shrub layer, reducing mulching and watering, and ensuring that the lawn is kept mown low. Bandicoots, the main host of the Paralysis tick, can be kept out of the backyard through the use of animal exclusion fencing. This needs to go below the ground surface by 0.5m so that the animals cannot dig underneath. If ticks continue to be a problem, then insecticide control is an option. Currently the only registered insecticide for the control of the Paralysis tick in NSW is Brigade. Only a licensed pest controller can apply this chemical.

Tick Removal If a tick is detected that is attached, never attempt to place any chemical such as methylated spirits onto the tick, nor should it be touched or disturbed, as the tick will inject saliva into the skin, which could make the situation worse. Rather the tick should be sprayed with an aerosol insect repellent preferably containing pyrethrin or a pyrethroid (if a repellent cannot be found which contains a pyrethroid, then Lyclear, a scabies cream containing permethrin will work fine). The combination of hydrocarbons and the pyrethrin acts as a narcotic and a toxicant, and prevents the tick from injecting its saliva. The tick should be sprayed again one minute later (or dabbed with the Lyclear) and left. After 24 hours it should drop off naturally or be gently removed with fine-tipped forceps. It is normal for a tick bite to remain slightly itchy for several weeks, however if other symptoms develop, then a doctor should be consulted immediately.