Malaria Vector
Anopheles Gambiae
Malaria Symptoms
-Symptoms caused by RBC’s bursting
ii) 1st 4-6 hours: chills, sweats, headache
iii) More severe symptoms: nausea, vomiting, diarrhea, anemia, muscle/joint/back pain, dry cough
iv) In serious cases: Plasmodium Falciparum cases that can sometimes lead to kidney failure (black water fever), brain damage, coma, death
Malaria Pathogen
Plasmodium Falciparum: malignant, most cases in africa, no relapses
Plasmodium Vivax: benign, most cases in asia, relapse cycle
Malaria Life Cycle
IN VERTEBRATE: mosquito injects hypozoite (vivax) or sporozoites that mature in liver > mature liver schizont bursts & merozites find RBC’s to burst . merozites form erythrocytic schizont that forms an erythrocyte then a gametocyte
IN MOSQUITO: mosquito takes up gametocytes > finds a zygote to form Ookinete > forms Oocysts on midgut then rupture and release sporozoites > go to salivary glands where can reinfect vertebrates
Malaria Control
IRS, bed nets, distribution of Chloroquine
Yellow Fever Vector
Aedes Aegypti (also vector of Dengue fever)
Yellow Fever Symptoms
a) 3-6 day intrinsic incubation period
b) Most infected cases are asymptomatic
c) More serious cases (15% of ppl infected)
i) 1st Phase: high fever, headache, nausea, vomiting
ii) 2nd Phase (Toxic Phase): mortality rate = 20-50%
(1) Jaundice: when liver is damaged
(2) Black Vomit: internal bleeding
Yellow Fever Primates in Africa
are Reservoir hosts, where they do not die and YF is spread year-around so its endemic, Rural Cycle occurs
Yellow Fever Primates in South America
are Amplifying host, so they do die and YF is sporadic, so its epizootic, NO Rural Cycle
Yellow Fever Control
Vaccine available since 1937, Yellow Fever could never be eradicated because it is maintained in the zoonotic cycle in primates, therefore without killing all primates eradication would be impossible.
West Nile Vector
a) Culex Pipens(northern house mosquito)
b) Culex Quinquefasciatus(southern house mosquito)
West Nile Symptoms
a) 80% asymptomatic
b) 20% develop West Nile Fever: fever, headache, aches, can last several weeks.
c) Severe disease: those who do recover suffer brain dmg. and never the same.
i) West Nile Encephalitis: swelling of the brain?
ii) West Nile Meningitis: swelling of the brain & membrane surrounding it
iii) West Nile Meningoeencephalits (both Encephalitis and Meningitis)
West Nile Bridge Vector
West Nile Prevention
insect repellent: DEET, eliminate standing water, window/door screens, mosquito fish in pools of water
Lymphatic Fileriasis Vector
Culex Quinquefasciatus, Anopheles vectors, Aedes vectors
Lymphatic Fileriasis Pathogen
Wuchereri Bancrofti = 91% of time
Brugia = 9% of time
Lymphatic Fileriasis Life Cycle
L3 larvae enter skin when female takes blood meal; mosquito ingests microfilaria during blood meal to get infected
Lymphatic Fileriasis Symptoms
– caused by accumulation of DEAD filarial worms
a) Phase 1: asymptomatic but many have microfilaria in blood, these people are reservoir host.
b) Phase 2: (acute) adult worms invade lymph nodes & filarial episodic fevers occur.
c) Phase 3: (chronic) lymph channels blocked by dead worms so there’s a buildup of fluid>extension of limbs, area is filled with scar tissue (e.g. Chyluria and Lymphoedema)
i) Chronic disease, ONLY in humans, must accumulate a # of ADULT worms before symptoms/severity occur
Lymphatic Fileriasis Treatment
a) Ivermectin: kills microfilaria, which is great for stopping spread, but dead microfilariae worms are what cause damage.
b) Albendozole: effective against adult worms, side effects occur because of immune system’s reaction to dead worms
River Blindness Vector
River Blindness Pathogen
Onchocerca Volvulus
Simuliidae (Diptera) Control for River Blindness
a) only females blood feed and are daytime feeders> no bed nets or IRS or other good control methods
b) Most effective way: targeting larvae by larviciding rivers with insecticides, (ex. BTI: bacteria used to kill larvae)
c) Onchoceriasis Control Program (OCP): failed attempt at eradicating river blindness, but did prevent many cases, from 1974- 2002
d) African Programme for Onchocercias Control (OPAC)
e) Onchocerciasis Elimination Programme for the Americas (OEPA)
River Blindness Life Cycle
L3 larvae enter bite wound which infects humans; blackfly ingests microfilaria which infects blackfly (microfilaria stay under skin, NOT in bloodstream like LF)
River Blindness Symptoms
(must be infected by multiple microfilariae that die before severe symptoms occur)
a) Nodules: caused by J3 larvae that gets inoculated in skin & mature to adults
b) Skin disease: microfilariae in skin cause tissue reaction, unbearable itching, “lizard skin”
c) Eye disease: damage occurs when microfilariae die in eye
d) Hanging Groin: caused by microfilariae in lymph system, connective tissue is broken down
River Blindness Treatment
a) DEC is too dangerous in river blindness> too many side effects
b) Ivermectin : prevents females from producing microfilaria
c) River blindness could be eradicated, conditions for mass drug administration include: highly effective drug needs to be available, long acting, safe, & cheap
Sleeping Sickness Vector
Tsetse fly
Family: Glossinidae
– Glossina morsitans: East Africa
– Glossina palpalis: West Africa
Sleeping Sickness Pathogen
a) Trypanosoma brucei brucei >only in animals
b) Trypanosoma brucei gambiense > West Africa (chronic); human ONLY
c) Trypanosoma brucei rhodesiense > East Africa (acute); zoonosis; in savanna, NOT as common as West African HAT
Sleeping Sickness Treatment
a) for Stages 1 & 2:
i) Pentamidine for Trypanosoma brucei gambiense
ii) Suramine for Trypanosoma brucei rhodesiense
b) for Stage 3: (parasites in brain):
i) Melarsoprol>side effects fatal in 3-10% of cases
ii) Eflornithine>56 I.V.s needed, production stopped b/c drug wasn’t profitable, now is donate to African nations
Sleeping Sickness Control
a) Vector Control: traps (biggest form of tsetse fly control), insecticide treatment by spraying cattle, sterile insect release: tons of sterile males > females have less offspring island location is necessary b/c tsetse have to be only species in region
b) Screening of population and treat infected individuals ex. Angola in 1950 12 mill. were screened annually (entire population) on 3 cases identified then a resurgence occurred because of civil war.
c) Slaughter wildlife: because they’re hosts
d) Clearing of land: remove brush because they’re breeding habitats
Sleeping Sickness (Trypanosoma brucei) Life Cycle
a) In Human: tsetse fly takes blood meal>trypomastigotes transform into bloodstream> trypomastigotes multiply and are found in blood, lymph, and spine fluid
i) Trypomastigotes > form its adapted to best live in humans
b) In Tsetse fly: tsetse fly ingests trypomastigotes>trypomastigotes multiply in fly’s midgut>trypomastigotes leave midgut and transform into epimastigotes>epimastigotes multiply in salivary gland and transform into trypomastigotes
i) Epimastigotes> form its adapted to best live in tsetse fly
Chagas Vector
Kissing Bug: feed at night, prefer to live in or close nearby houses but can go months without a meal; both male and female and all stages blood feed>greater chance of picking up and transmitting infections; juvenile bug looks same just smaller than adult. Two highly domesticated species:
a. Triatoma Infestans > South America
b. Rhodnius Prolixus > Central America
Chagas Pathogen
Trypanosoma Cruzi
Chagas Transmission
a. Blood transfusion is most common way in north America
b. Kissing bugs defecate when feeding and T. Cruzi is now on host, once host itches the bite wound, T. Cruzi gets into the body
Chagas (Trypanosoma Cruzi) Life Cycle
Only when kissing bug defecates does host get infected from itching wound
a. In Vector: take up trypomastigote>Epimatigote > trypomastigote
b. In Human: trypomastigote > amastigote > trypmastigote (infects humans and goes inside cells
Chagas Treatment
more effective the earlier diagnosed
a. For acute phase: anti-parasite treatment drugs often not effective and are fairly toxic.
b. For chronic phase: pace makers, drugs for irregular heartbeat, Chagas is common reason for heart transplant, surgery for mega colon etc.
Chagas Symptoms
a. Acute Phase: asymptomatic; acute inflammatory reaction at site of parasite entry, If around eye called “sign of Romana”; shares many general disease symptoms, rare but heart muscle can be invaded and lead to heart failure
b. Chronic Phase: occurs in ~30% of adults who survive acute phase, this occurs years (10-30) after infection, parasites invade organs of body, nerve cells controlling esophagus and colon can be destroyed causing no peristaltic movements
Chagas Control
a. Vector Control: IRS because they like to high in houses
b. Blood bank screening
c. Prenatal screening
Leishmaniasis Vector
Sand Fly
2 medically important genera:
a. Phlebatomus > old world
b. Lutzomyia > new world
Leishmaniasis Pathogen
Leishmania Reservoir Hosts
a. For Cutaneous: rodents (main), hyraxes, dogs
b. For Visceral: dogs are main reservoir host
Leishmania Life Cycle
a. In humans: sand fly takes blood meal, promastigote are phagocytized by macrophages which transform in amastigotes that multiply in cells of various tissues
b. In sand fly: sand fly takes blood meal and ingests parasitized cell, amastigotes transform into promastigotes then divide and migrate to proboscis
Leishmaniasis Transmission
a. Sand Fly bites
b. Congenital (mother to fetus)
c. Blood transfusion
Leishmaniasis Stages
6. Cutaneous Leishmaniasis:
a. most common form; symptoms may occur years after infection, seldom affect same person more than once.
b. Unsightly scar, “pizza-like” lesion
7. Muco-Cutaneous Leishmaniasis:
a. Initially a cutaneous lesion, but after months or years, chronic ulcers appear that affect skin and mucous layers and destroy cartilage of the nose. Severe disfigurement
8. Visceral Leishmaniasis:
a. Parasites migrate to bone-marrow, liver, and spleen
b. Almost always fatal if left untreated, patients often very susceptible to other infections, frequent cause of mortality.
Leishmaniasis Treatment
a. Cutaneous leishmaniasis
i. In old world: local or no treatment
ii. In new world: systemic treatment with drugs
b. Muco-cutaneous & Visceral Leishmaniasis
i. Systemic treatment & surgery for muco-cutaneous leishmaniasis
Leishmaniasis Control and Prevention
a. Control is often a by-product of malaria control
b. IRS in and around dwellings
c. Bed nets
d. Control reservoirs: dogs and rodents
e. Infection with L. major on aesthetically less important part of body
Leishmaniasis Key Points
a. Sand fly saliva enhances infection with Leishmania
b. Different strains of sand fly injecting the same parasite can cause different disease
c. Prior exposure to sand fly bites immunizes (partially) to infection with Leishmania
Lyme Disease Vector
a. Ixodida (Hard Ticks)
i. Ixodes Scapularis> East Coast
ii. Ixodes Pacificus> West Coast
Lyme Disease Pathogen
Borrelia burgdorferi in US
Lyme Disease Reservoir Host
white footed mouse, NOT deer (deer do support Ixodes Scapularis populations but are not reservoir host for lyme)
Lyme Disease Symptoms
i. Stage 1: early localized infection, erythema chronicum migrans, “bulls-eye” rash
ii. Stage 2: early disseminated infection, borrelia begins to spread through bloodstream and erythemia (dark red splotches on body) may develop across the body
iii. Stage 3: late persistent infection, untreated patients may develop severe and chronic symptoms affecting: brain, nerves, joints, heart
Lyme Disease Treatment
i. Anti-biotics: patients treated earlier have best results
ii. Controversy over anti-biotics used for long term chronic patients, because doctors/scientist say it doesn’t help but some patients disagree
Lyme Disease Prevention
i. Rapid tick removal, reduce primary hosts, vegetation reduction, fences around yards, spraying acaricides, treating deer with acaricides
The Plague Vector
rat flea, Xenopsylla cheopis; fleas are endopterygota (wingless), both sexes blood feed and don’t remain on host but nearby, larvae feed on organic debris
The Palgue Pathogen
Yersinia Pestis
The Plague Reservoir Host
rats (plague is a zoonosis)
The Plague Transmission
most common mode of transmission is through flea bite
a. Sylvatic Cycle: in forest, direct contact with infective rodent can cause transmission
b. Bubonic Plague: transmission commonly by infective flea or direct contact with wild infective rodent
c. Pneumonic Plague Epidemic: plague bacteria in lungs, and can now spread from human>human
d. Urban Cycle (Urban Epidemic): sylvatic cycle is transmitted to domestic rats> rats die> fleas feed on humans
The Plague 3 forms
i. The Bubonic Plauge: enlarged, tender lymph nodes; 50-90% fatal if not treated > often progresses to Septicemic/ Pneumonic Plague
ii. Septicemic Plague: blood starts clotting> organs don’t get any oxygen> organ failure; mortality rate is almost 100%, sometimes progress to Pneumonic Plague
iii. The Pneumonic Plague: coughing blood > can cause human to human transmission; mortality close to 100%
The Plague Medical Significance
a. Nuisance: most commonly cause by cat flea, irritation and itching of skin, some cause allergic reactions
b. Murine Typhus (endemic typhus) (Rickettsia typhi)
c. Cestodes (tape worms): larvae eat worm eggs and worms multiply in fleas and infect pets, people get infected with contact with pet
d. Cat Scratch Disease: usually cures itself, not serious
e. Tunga Penetrans (Jigger, Chigoe, or Sand Flea
f. The Proventriculus: Yersinia Pestis produces a clot that blocks alimentary canal of Xenopsylla Cheopis> this starves flea and induces it to bite frequently> increases vectorial capacity > tryig to swallow the flea will regurgitate blood bacteria (even greater chance of infection)