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BIOWEATHER Pests : locust plagues Parasites : worms, flukes and spirochetes Diseases : ‘emerging’ viruses. “Feeling under the weather?”. Locusts and grasshoppers in Africa. Desert Locusts.
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BIOWEATHER Pests: locust plagues Parasites: worms, flukes and spirochetes Diseases: ‘emerging’ viruses “Feeling under the weather?”
Desert Locusts Locusts eat their own weight (about 4 g) in plant matter per day; a swarm may consist of a billion insects, and 100 swarms may be on the move during a plague (eating 400 kilotons per day). A swarm can fly 300 km in one day, remain afloat out at sea (and take off again), and remain active even when covered by snow.
juvenile egg solitary hopper gregarious locust Source: BBC website
Last major locust plague (1987-89) Outbreak: 1967-68. Drought in Africa in 1970’s and early 80’s produced a recession in the locust cycle. Heavy rains in 1987-89. In Jan. 1987 large swarms formed in Saudi Arabia. Despite the Saudis’ massive control efforts some of the swarms crossed the Red Sea and gradually moved west to Mauritania and north to Algeria. Western Sahara had heavy rains, and threat to the states in North Africa was so grave that Morocco deployed 200 000 soldiers to combat the swarms. Strong winds aloft (associated with Hurricane Joan) carried some of these locusts across the Atlantic to the Caribbean in October 1988. They reached as far west as Jamaica.
Upsurges in 1990’s 1996-1998: Local upsurge in Red Sea Basin (from Yemen - Saudi Arabia to Sudan - Ethiopia - Somalia -Eritrea)
a b 2004 outbreak Nov. CYPRUS, EGYPT c map of outbreak b) swarms in Mauritania Aerial spraying in the western Sahara Source: BBC website
Monthly snapshots of outbreaks from Nov. 2003-Nov. 2004 gregarious adults gregarious juveniles
Rainfall and the Australian plague locust 2004 plague Scale of outbreak Sources: BBC website; www.affa.gov.au; www.bom.gov.au/silo/products/cli_chg
Combating locusts • Good news: • Prediction of swarm development and movements much easier with satellites which can identify areas of new plant growth and wind patterns in remote desert areas. • Aerial spraying of young (pre-swarm) populations with insecticide (e.g. malathion) is still effective. • New biopesticide (Metarhizum fungus = “Green Muscle”) kills locusts and grasshoppers in 3 - 4 weeks. • Trigger for gregarious behaviour (hind leg stimulation!) recently identified; may lead to suppression techniques. • Locusts are more nutritious than beef - “Cooking with Sky Prawns” (20 recipes for cooking locusts from Australia)
Combating locusts • Bad news: • Highly cyclical nature leads to poor maintenance of surveillance and control equipment during recessions. • Political conflicts create refuge areas for swarms: The western Sahara desert is littered with land mines from the Polisario war.Morocco-Algeria-Libya are reluctant to cooperate;The Sudan is currently in the midst of a civil war; locust control is not a priority for the local government or for international humanitarian agencies.
Malaria (Ital: “bad air”) 1990’s: 2 000 M people at risk 300 M are infected 110 M cases reported annually (85% in Africa; 7% in SE Asia) Deaths: 1 - 2 M annually Vector: Anopheles mosquito (50-60 spp of the 380 known species of anophelines) can carry the parasites. Parasites: Four species of Plasmodium. P. falciparum causes most severe symptoms. Symptoms: high fever, dehydration, death in severe cases
Global incidence of malaria Map area equivalent to cases per 100 people (92% of all cases in Africa) Source: www.worldmapper.org/posters/worldmapper_map229_ver5.pdf
The malaria transmission cycle I http://www.cdc.gov/malaria/biology/life_cycle.htm
The malaria transmission cycle II After a single sporozoite (the parasite form inoculated by the female mosquito) of Plasmodium falciparum invades a liver cell, the parasite grows in 6 days and produces 30,000-40,000 daughter cells (merozoites) which are released into the blood when the liver cell ruptures. In the blood, after a single merozoite invades a red blood cell, the parasite grows in 48 hours and produces 8-24 daughter cells, which are released into the blood when the red blood cell ruptures. These male and female gametocytes are ingested by the mosquito during a blood meal, and inoculation of sporozoites begins again in the mosquito. http://www.cdc.gov/malaria/facts.htm
Role of climate in malaria outbreaks Moisture: Breeding success of mosquitoes is maximised in nutrient-rich pools; populations are most abundant in wet weather. Too much rain, however flushes pools and reduces breeding success. At temperatures between 25-30°C the malarial parasites and mosquito larvae mature quickly, the adult mosquitoes live longer, and female mosquitoes feed more frequently.
Temperature-controlled development of Plasmodium 4 P. malariae 3 Length of the life-cycle in anophelines (weeks) 2 P. falciparum P. vivax 1 optimal 0 15 20 25 30 Temperature (°C) minimum maximum
Sri Lanka (Ceylon):topography and annual precipitation (mm) 1000 1500 >2000 Summer monsoon
Malaria epidemic Sri Lanka (Ceylon) 1934-5 Malaria hyperendemic in dry north of island but rare in wet south (heavy rains flush mosquito larvae away). Southern population has little natural immunity. Drought in 1934-5 resulted in major epidemic in south. 30% of population fell ill; 80,000 died. Illustrates Ross’s “math of malaria” (~25d fever cycle) 1000 100 10 1 cases 0 25 50 75 days
The East African malaria resurgence:is climate change to blame? Kericho Kabale Gikonko Muhanga Months suitable for P. falciparum transmission Hay et al., (2002) Nature415, 905 - 909
Malaria resurgence ….. and decline 2005-6 ~10 000 cases in South Africa 2006-7 ~3 000 cases in South Africa
Why was malaria widespread in northern Europe in the LIA? Little Ice Age from: Reiter, P. 2000. "From Shakespeare to Defoe: Malaria in England during the Little Ice Age” Emerging Infectious Diseases vol. 6
Bilharzia (Schistosomiasis) • Infection caused by parasitic flatworms [“flukes”] in the genus Schistosoma. • Freswater snails are the intermediate hosts. Infection occurs through skin whilst wading in water. Eggs released by humans defecating or urinating near these bodies of water. • Victims become emaciated and very weak. • Common in areas such as the Nile Valley for several thousand years. Incidence varies with intensity of flooding in (sub)tropical lowlands.
Bilharzia: flukes, intestinal worms anda severe symptoms (enlargement of the liver and spleen)
Lyme Disease • Infection caused by bacterial spirochetes (Borreliaburgdorferi) transmitted by blood-sucking ticks. • Symptoms include arthritis, heart problems and severe neurological/nerve disorders. • Discovered in USA in 1975 (Lyme, CT) • Continued to increase and spread since surveillance began in 1982. • Lyme disease has global distribution in temperate areas. • Complex ecology linked to climate and land-use changes.
Deer ticks (Ixodes species) N.B. - The “dog tick” is not a member of the Ixodes genus and cannot spread Lyme disease
Why has incidence of Lyme disease increased in New England in the last 25 years? • Farm abandonment in early decades of last century. • Abandoned farmland undergoes ecological succession to oak-maple forest in about 50-80 years. • Expansion of suburban development into rural areas around NYC-Boston. • Reduced hunting of deer?
Viral disease transmission Ecology of flavivirus outbreaks (e.g. dengue, West Nile encephalitis) Ecology of bunyavirus outbreaks (e.g. sin nombre) Climate and viral disease
Emerging viruses FamilyDisease Vector and Reservoir
Dengue (hemorrhagic) fever • Inter-human transmission of DF by mosquito (esp. Aedes) bites. Fever lasts a few days. Complications can give rise to DHF (Fatal in >20% of cases if untreated). • DF cases common in humid (sub)tropical climates esp. in wet season (improved breeding success for Aedes).
World distribution of Aedesaegypti and dengue fever epidemics
Distribution of Aedesaegypti in the Americas 1995 Two decadesafter eradicationprogramme relaxed Prior to yellow fever eradicationprogramme. After post-war yellow fever eradicationprogramme.
Prior to 1981 1981- 1995 Distribution of dengue in the Americas
West Nile virus • West Nile virus is a strain of flavivrus, closely related to Japanese encephalitis. Previously reported from Africa and adjacent areas of southern Europe and western Asia. Previous outbreaks in Israel, France and S. Africa. and Romania (1996; 450 cases, 39 deaths). • It joins at least four other encephalitis viruses in North America, one of which [St. Louis encephalitis] is widespread. • Likely introduced into N. America by an infected international traveler or as a result of the importation of exotic birds.
fever, aches, stupor, (brain lesions, coma, paralysis, death?) direct transmission?