TICK-BORNE DISEASES

M. G. R. Varma

4.1 Tick-borne virus diseases

4.1.1 Colorado Tick fever (CTF)

Pathogen: Colorado Tick fever virus, Family Reoviridae, genus 
Orbivirus

Vectors: Dermacentor andersoni, Family Ixodidae

Reservoirs: Various small mammals, particularly the golden mantled 
ground squirrel (Spermophilus lateralis), Colombian ground squirrel 
(Citellus colombianus), yellow pine chipmunk (Eutamias amoenus) 
and least chipmunk (E. minimus).

A zoonosis acquired from a focal ecological niche. Foci exist in the Rocky Mountain states, South Dakota and in western Canada. In man it exhibits as a febrile illness with an exceptionally enduring viraemia and no skin rash, the latter differentiating it from Rocky Mountain spotted fever transmitted by the same species of tick. Although Dermacentor andersoni is the principal vector, the virus has been isolated from other species of ixodid ticks. Small mammals and immature D. andersoni maintain the infection in natural foci.Transmission to man is usually by bite of adult infected ticks. The virus is passed trans-stadially in ticks, but there is no evidence of transovarial transmission and the long (overwinter) persistence of the virus in ticks and rodents account for its maintenance in nature. In humid mountainous areas where rodents and ticks are numerous, the incidence of the infection in D. andersoni is 10% or higher.

4.1.2 Louping ill (Ll)

Pathogen: Louping ill virus, Family Togaviridae, genus Flavivirus

Vector: Ixodes ricinus, Family Ixodidae

Reservoirs: sheep, red deer (Cervus elaphus), red grouse 
(Lagopus scoticus)

A biphasic meningoencephalomyelitis principally affecting sheep, but also cattle, red grouse, red deer and man in rough hill pasture in the British Isles. Ixodes ricinus is the only known vector; its typical biotopes are areas where the soil remains damp throughout summer, as in poorly drained hill pastures. The tick also occurs in forests in the South of England as well as on continental Eurasia, but is infected with louping ill virus only in Britain and Ireland. A variety of small mammals and ground frequenting birds serve as hosts of the immature tick. Sheep, red deer and cattle are the major hosts of adult ticks. Human cases occur among people with close contact with sheep and tick biotopes, e.g., shepherds and abattoir workers. Transmission to man is by bite of infected ticks. There is trans-stadial passage of virus but transovarial transmission has not been demonstrated.

4.1.3 Encephalitides

Tick-borne encephalitis (TBE) (= Far Eastern or Russian Spring-Summer encephalitis (RSSE), Central European or Western tick-borne encephalitis (TBE), biphasic meningoencephalitis, diphasic milk fever)

Pathogen: TBE virus, Family Togaviridae, genus Flavivirus

Vectors: Ixodes ricinus (Western form, TBE); I. persulcatus 
(Far Eastern form, RSSE), Family Ixodidae

Reservoirs: Small mammals; ticks through transovarial transmission

The Far Eastern form, often referred to as Russian Spring-Summer encephalitis (RSSE), is associated with the taiga forest and is transmitted chiefly by Ixodes persulcatus. This tick is intimately associated as larvae and nymphs with many small forest mammals and birds, and as adults with larger wild and domestic mammals. The tick requires 2-4 years to complete its life cycle. In western USSR and in eastern and western Europe, it is replaced by I. ricinus, the chief vector of the western type of tick-borne encephalitis. In the coniferous and temperate deciduous forests of eastern Europe extending from the Urals to the Atlantic Ocean, I. ricinus is the most common tick species. In western USSR, the ranges of the two species overlap and both types of the disease may occur. Other tick species may be involved to a minor extent and transmission is possible by drinking infected goats' milk as well as by tick bite.During the 1960s, up to 80% of RSSE cases were in residents within a 3-8 km radius of their homes, contracted during holidays and weekend trips to the forests, a major pleasure for city-bound people. The reported "spread" of TBE in western Europe is almost certainly due to increased man-tick contact following an increase in leisure and sporting activities which bring man into infected biotopes.
Wandering and migrating birds may spread the ticks into new localities. The viruses are maintained in their tick vectors by trans-stadial passage and by transovarial passage to succeeding generations.

4.1.4 Kyasanur Forest disease (KFD)

Pathogen: KFD virus, Family Togaviridae, genus Flavivirus

Vectors: Ticks of the Family Ixodidae, principally Haemaphysalis 
spinigera and H. turturis

Reservoirs: Possibly monkeys and small rodents

The disease was discovered in Kyasanur Forest in South India in 1957 following investigations of deaths of monkeys, Presbytis entellus and Macaca radiata in the forest and first suspected to be jungle yellow fever. Human infection with a high mortality in the initial outbreaks, was always associated with activities such as wood gathering and cattle grazing in the forests.The most abundant tick species in the enzootic area is Haemaphysalis spinigera, the major vector responsible for epizootics and epidemics of the disease. H. spinigera is widely distributed in the tropical evergreen/deciduous forests of southern and central India and Sri Lanka. KFD virus has been isolated from seven other species of Haemaphysalis as well as from Dermacentor and Ixodes ticks.
Larvae and nymphs of Haemaphysalis spinigera parasitize several species of small forest mammals and birds as well as monkeys. Cattle are heavily parasitized by adults of H. spinigera and help to amplify the tick population. Neither cattle nor birds are thought to have any significant role in virus maintenance, apart from acting as hosts for the vector ticks. Man is parasitized almost exclusively by larvae and nymphs of H. spinigera and in the absence of natural transovarial transmission of the virus in this species, transmission to man is by bite of infected nymphal ticks. Other Haemaphysalis spp., particularly H. turturis maintain the enzootic cycle.
Most human cases occur during the dry months of March to May, following months of peak nymphal tick activity. Since the original outbreak of 1957, outbreaks in other forested areas, all in southern India have occurred, almost certainly due to deforestation/exploitation and the entry of man into already existing foci of infection.
INDEX OF MAPS
The maps listed below are presented on pages 64 and 65.
MAP 21 Distribution of Colorado Tick fever and of Dermacentor andersoni
MAP 22 Distribution of louping ill, tick-borne encephalitis, Russian Spring-Summer encephalitis and Kyasaur Forest disease and their main vectors.

4.2 Tick-borne borrelioses

4.2.1 Tick-borne relapsing fever (= tick-borne spirochaetosis, endemic relapsing fever)

Pathogen: Borrelia spp., about seven species cause disease in 
man.

Vectors: Soft ticks of the Family Argasidae, genus Ornithodoros.

Reservoirs: Ornithodoros ticks, through transovarial transmission.

In the Old World, the disease is endemic in East, central and South Africa, the Mediterranean region (Portugal, Spain, North and West Africa) extending eastwards through Cyprus, Israel, Iran, Central Asia, Kashmir (India) to western China (Map 23, page 66). In the New World, it occurs in central and western USA, Middle and South America southwards to northern Argentina (Map 24, page 67). Several hundred human cases are reported annually. The mortality is seldom high, but morbidity may be severe. It is effectively treated with antibiotics.Foci of infection are usually restricted and include huts, caves, stables, piggeries, other animal shelters, resort cabins. Trans-stadial and the high rate of transovarial transmission and the ability of the vector ticks to starve for long periods lead to perpetuation of natural foci in the absence of vertebrate hosts.
Rodents probably act as amplifiers rather than as reservoirs of the infection. Following an infecting feed, the ticks have a disseminated infection of practically all the internal organs. Transmission usually through salivary secretion containing the pathogens, and through contamination of the bite wound through infective coxal fluid produced by feeding ticks just before detachment. Vector species which do not produce coxal fluid while on the host, transmit solely by bite. In contrast to ixodid ticks, the argasid ticks (Ornithodoros) are rapid feeders.

4.2.2 Erythema borreliosis migrans (= erythema chronicum migrans, Lyme disease)

Pathogen: Borrelia burgdorferi.

Vectors: Ixodes spp., I. ricinus in Europe, I. dammini in 
north-eastern USA, I. pacificus in California and probably I. holocyclus 
in Australia.

Amblyomma americanum is a possible vector in USA.

Reservoirs: Rodents and deer.

The disease was first recognized in Sweden in 1909 and later reported from Austria and other parts of continental Europe. It appeared in the USA in 1970 and caused an epidemic outbreak of arthritis in New England in 1972 in Old Lyme which led to the entity being named first Lyme arthritis then Lyme disease. In 1977 it was reported in the United Kingdom and in 1982 in Australia (Map 25, page 68).In man the disease is manifested by a dermatosis with a subsequent arthritis, neuropathological manifestations and cardiac involvement. Antibiotics in large doses are curative.
In Europe I. ricinus is widespread with about 100 mammalian, avian and reptilian hosts, living in forest environments under 1200 m altitude.
There is some doubt whether there are some differences in Borrelia burgdofferi in Europe and that in USA though they are immunologically closely similar with shared antigenic determinants.
INDEX OF MAPS
The maps listed below are presented on pages 66 - 68.
MAP 23 Old World distribution of endemic tick-borne relapsing fever and the principal Ornithodoros vectors.
MAP 24 New World distribution of endemic tick-borne relapsing fever and the principal Ornithodoros vectors.
MAP 25 Distribution of erythema borreliosis migrans (Lyme disease) and its major vectors.

4.3 Tick-borne rickettsioses

4.3.1 Rocky Mountain spotted fever (= RMSF, Mexican spotted fever, Tobia fever, Sao Paulo fever)

Pathogen: Rickettsia rickettsi.

Vectors: Ticks of the Family Ixodidae; Dermacentor andersoni 
(the Rocky Mountain wood tick), D. variabilis (the American dog 
tick), Amblyomma cajennense (the Cayenne tick).

Reservoirs: Primarily ticks, transovarial transmission common; 
also small mammals, especially rodents.

Rocky Mountain spotted fever is a zoonotic infection widely distributed in the Nearctic and Neotropical regions from Canada to South America, now mostly prevalent in eastern USA where the mortality and morbidity rates remain unacceptably high (Map 26, page 69). With the advent of antibiotics, the mortality rate in human beings has been reduced. In parts of eastern USA, with an increasing human population and the encroachment of residential areas into abandoned fields and woodland with considerable rodent and tick activity, the attack rate is high and women and children account for at least half of the reported cases; most cases in eastern and southern USA are rural and suburban. Apart from the three species of ticks mentioned above, others, particularly Rhipicephalus sanguineus have been found naturally infected, and may be involved in the maintenance of natural foci of infection and the transmission of infection to man.Immature stages of Dermacentor andersoni and D. variabilis feed on small mammals; D. andersoni adults attack large wild and domestic herbivores and D. variabilis prefers wild and domestic carnivores; both species feed secondarily on other mammals, including man.
Any stage of a tick vector can acquire the infection by feeding. There is transstadial and transovarial transmission of the pathogen in ticks. Transmission to mammals is by the bite of infected ticks; in the case of infected ticks which have overwintered, it may require a day or two for the pathogen to be reactivated and for transmission to take place. Heavy infection in ticks may sometimes be fatal for engorged female vector ticks and may reduce oviposition and egg development.

4.3.2 Boutonneuse fever (= South African tick typhus, Kenya tick typhus, Marseilles fever, Crimean tick typhus, Indian tick typhus); Siberian tick typhus (= North Asian tick typhus); Queensland tick typhus

Pathogen: Rickettsia conori(Boutonneuse fever), R. sibirica 
(Siberian tick typhus), R. australis (Queensland tick typhus).

Vectors: Ticks of the Family Ixodidae.

Reservoirs: Ticks and rodents.

Boutonneuse fever is known by various local names and is widely distributed in Africa, including Egypt, where it was recently found. It also occurs in the European and African areas near the Mediterranean and in Israel, and over much of southeastern Asia. The name is derived from the button-like lesion at the site of attachment of the tick.The chief vectors are Amblyomma hebraeum (in the South African veld) and Rhipicephalus sanguineus. In France, the disease is so closely associated with rabbits that the incidence dropped considerably following decimation of the rabbit population by myxomatosis. There is transovarial transmission and transmission to man is by tick bite. Infection may also occur by contact of the hands with the skin or eyes after crushing ticks removed from dogs. Urban cases appear to be associated with dogs and dog ticks.
Siberian tick typhus has a wide distribution from the far eastern Pacific through northern and southern Siberia, Mongolia, Kazakh and Kirgiz Republics to the Armenian Republic of the USSR. The disease was first recognized in the 1930s when virgin steppe was extensively colonized. Nine tick species have been reported to be reservoirs and vectors of R. sibirica, the most important being Dermacentor marginatus, D. silvarum, Haemaphysalis concinna and Rhipicephalus sanguineus, the last named being the vector in the western part of the distribution of the disease. There is transstadial and transovarial passage of the agent in ticks and transmission to man is by tick bite.
Queensland tick typhus is related to the rickettsialpox spotted fever caused by R. akari transmitted by mites. It is restricted to dense forest interspersed with grassy savanna or secondary scrub. The vector Ixodes holocyclus is widely distributed in coastal and densely forested areas of Australia and is an unusually indiscriminate feeder, causing tick paralysis. There is some evidence that the tick can transmit the infection by bite within a matter of hours after attachment.
INDEX OF MAPS
The maps listed below are presented on pages 69 and 70.
MAP 26 Distribution of tick-borne typhus fevers (Rocky Mountain Spotted Fever) and their vectors in the Americas.
MAP 27 Distribution of tick-borne typhus fevers of the Old World and their vectors.
REFERENCES
Ackermann, R. Erythema migrans borreliosis in Europe: clinical picture, diagnosis, therapy. IXth International Congress of Infectious and Parasitic Diseases, Munich, July 20-26, 1986. Abstract 1210. Munich, Futuramed.
Aeschlimann, A. Ixodes ricini, Linn,1758 (Ixodoidea: Ixodidae). Essai preliminaire de synthase sur la biologie de cette espece en Suisse. Acta Tropica, 29: 321-340 (1972).
Anastos, G. The ticks, or ixodides, of the USSR, . Washington DC, US Public Health Service, 1957, 397 pp.
Blaskovic, D. Studies on tick-borne encephalitis. Bulletin of the World Health Organization, 36 (suppl. 1),1-94 (1967).
Burgdorfer, W. A review of Rocky Mountain spotted fever (tick-borne typhus), its agent, and its tick vectors in the United States. Journal of Medical Entomology, 12: 269-278 (1975).
Burgdorfer, W. The epidemiology of the relapsing fevers. In: Johnson, R. C., ed. "The biology of parasitic spirochetes." New York, Academic Press,1976, pp.191-200.
Burgdorfer, W. Ecological and epidemiological considerations of the Lyme disease spirochaete, Borrelia burgdorfersi. In: Proceedings IXth International Congress of Infectious and Parasitic Diseases, Munich, July 20-26,1986. Vol 11, 11-15, Munich, MMV Medizin Verlag,1986.
Cooley, R.A. The Rocky Mountain wood tick. Montana State College Experimental Station Bulletin, No. 268, (1932) 58 pp.
Cooley, R.A. The genera Dermacentor and Otocentor (lxodidae) in the United States, with studies in variation. U.S. National Institute of Health Bulletin, No. 171, 1938, 89 pp.
Goubau, P. F. Relapsing fevers. A review. Annales de la Societe Belge de Medecine Tropicale, 64: 335-384 (1984).
Haworth, J. Erythema chronicum migrans. Travel Medicine Intemational, 4: 69-71 (1986).
Hoogstraal, H. Ticks in relation to human diseases caused by viruses. Annual Review of Entomology, 11: 261-305 (1966).
Hoogstraal, H. Ticks in relation to human diseases caused by Rickettsia species. Annual Review of Entomology, 12, 377-420 (1967).
Hoogstraal, H. Ticks and spirochetes. Acta Tropica, 36: 133-136 (1979).Annual Review of Entomology, 26: 75-99 (1981)
Indian Journal of Medical Research, 56 (4). April (Supplement). Eleven papers on Kyanasur Forest Disease, pp. 497-636 (1968).
Johnson, R. C., Schmid, G. P., Hyde, F. W., Steigerwalt, A. G. & Bremner, D. J. Borrelia burgdorferi sp. nov. Etiologic agent of Lyme disease. International Journal of Systemic Bacteriology, 34: 496-497 (1984) .
Leeson, H. S. Some notes on the recorded distribution of Old World species of Ornithodoros. Bulletin of Entomological Research, 44: 517-526 (1953).
Leeson, H. S. Further notes on the geographical distribution of Old World species of Ornithodoros. Bulletin of Entomological Research, 46: 747-748 (1956) .
Nosek, J. and Blaskovic, D. Ticks as vectors of tick-borne encephalitis (TBE) virus in Europe. In: Proceedings of Ill lnternational Congress on Acarology, Prague, pp. 589-591,1971.
Obasi, O. E. Erythema chronicum migrans. British Journal of Dermatology, 97: 459 (1977).
Petrischeva, P. A. & Skrynnik, A. N. Tick-bome relapsing fever. In: "Geography of natural focal diseases of man". Moscow, Medgiz, 1969, pp. 95-119 [In Russian].
Roberts, F. S.H . Australian ticks. Melbourne, CSI RO,1970, 267 pp.
Rufli, Th. "Lyme disease" der neuen Welt versus Erythema Chronicum Migrans der altem Welt und seine Komplikationen. Zentralblatt Hant. und Geschlech, Krankheiten, 150: 909-914 (1985).
Scrimenti, R. J. Erythemachronicum migrans. Archives of Dermatology, 102: 104-105 (1970).
Steere, A. C., Broderick, T. F. & Malawesta, S. E. Erythema chronicum migrans and Lyme arthritis: epidemiologic evidence of a tick vector. American Joumal of Epidemiology, 108: 312-321 (1978).
Stewart, A., Glass, A., Patel, A., Watt, G., Cripps, A. & Clancy, R. Lyme arthritis in Hunter Valley. Medical Journal of Australia, 1: 139 (1982).
Varma, M.G.R. The acarology of Louping III. Acarologia, fasc. H.S., pp. 241-254 (1964)
Varma, M.G.R. The distribution of Ixodes ricinus in Britain in relation to climate and vegetation. In: Theoretical questions of natural foci of diseases. Proceedings of a Symposium held in Prague,1963. Prague Publishing House of the Czech Academy of Sciences,1965.
Work, T.H. and Tropido, H. Kyanasur Forest Disease: a new infection of man and monkeys in tropical India by a virus of the Russian Spring-Summer Complex. In: Proceedings of the ninth Pacific Science Congress, 17. pp.80-84 (1957).

5. MITE-BORNE RICKETTSIOSIS

M.G.R. Varma

Chigger-borne rickettsiosis (= Tsutsugamushi disease, Japanese river fever, scrub typhus, mite-borne typhus)

Pathogen: Rickettsia tsutsugamushi (= R. orientalis).

Vectors: Mites of the Family Trombiculidae, Genus 
Leptotrombidium

Reservoirs: Mites, through transovarial transmission; various spp. 
of rodents, especially Rattus.

A zoonotic infection, first described from Japan, now known to occur over most of southeastern Asia, India, Sri Lanka, Pakistan, islands of the southwest Pacific, and coastal Queensland (Australia) (Map 28). It is found in a wide range of biotopes from flooded alluvial plains in Japan, scrub, and dense but disturbed forest in southeastern Asia, to semi-deserts as in Pakistan and alpine reaches in the mountains as in the Himalayas. The actual distribution may be much wider. A high incidence occurs in human beings exposed to infected biotopes. There were large outbreaks in nonimmune troops in southeastern Asia during the Second World War and the Vietnam War, with a high mortality.Larvae of the vector mites, chiggers (the only parasitic stage in the life cycle of the mites), acquire the infection by feeding on infected rodents. The rickettsiae are trans-stadially transmitted through non-parasitic nymphal and adult mites which are predatory on soil arthropods, and transovarially through the eggs to parasitic larvae of the next generation, which transmit the pathogen during feeding on animals and man. For most, but not all human cases, a lesion or "eschar" develops at the site of the infective chigger bite.
INDEX OF MAPS
The map listed below is presented on page 73.
MAP 28 Areas of endemic chigger-borne rickettsiosis and distribution of the Leptotrombidium vectors.
REFERENCES
Audy, J.R. A summary topographical account of scrub-typhus 1908-1946. Bulletin of the Institute of Medical Fesearch, Federation of Malaya, 1: 1-82 (1949).
Blake, F.G. et al. Studies on Tsutsugamushi disease (scrub typhus, mite-borne typhus) in New Guinea and adjacent islands. American Journal of Hygiene, 41: 293-373 (1945).
Tamiya, T. Recent advance in studies of Tsutsugamushi disease in Japan. Tokyo, Medical Culture Inc., 1962, 309 pp.
Traub, R. & Wisseman, Jr. C.L. Ecological considerations in scrub typhus. 1. Emerging concepts. Bulletin of the World Health Organization, 39: 209-218 (1968).
Traub, R. & Wisseman, Jr. C.L. The ecology of chigger-borne rickettsiosis (scrub typhus). Joumal of Medical Entomology, 11: 237-303 (1974).


http://www.ciesin.org/docs/001-613/001-613.html