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24 Cards in this Set
- Front
- Back
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Cholera
Symptoms |
– Classic example of severe
diarrhea • Can amount to loss of 20 liters of fluid per day – Often termed “rice water stools” due to appearance – Vomiting common in most cases • Usually occurs at the onset of disease – Many suffer muscles cramps • Caused by loss of fluid and electrolytes |
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Cholera
CausativeAgent |
– Vibrio cholerae
• Gram-negative • Curved bacillus • Salt tolerant • Tolerates high alkaline environment |
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Cholera
Pathofenesis |
– Large numbers must be ingested to effect disease due to sensitivity to stomach acid
– In small intestine, organisms adhere to epithelial lining and multiply there – Bacteria-produced toxin • Cholera toxin – Responsible for symptoms • A-B toxin – B fragment has no toxicity, serves to bind toxin to cells – A fragment responsible for toxicity, causes excess secretion of fluid – Toxin destroyed by heat |
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Cholera
Epidemiology |
– Fecal contamination of water most common
source of transmission • Crabs and vegetable fertilized with human feces have also been implicated – Person with cholera may discharge at least 1 million bacteria per milliliter of feces – “Rice water stools” |
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Cholera
Prevention |
– Depends largely on
• Adequate sanitation • Availability of safe water supplies – Travelers should cook food immediately before eating • Fruit should be peeled personally • Avoid ice unless made with boiled water |
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Cholera
Treatment |
– Treatment depends on rapid replacement of fluids and electrolytes
• Essential before irreversible damage to vital organs – Replacement of fluids and electrolytes decreases mortality to less than 1% |
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Dengue fever
Symptoms |
• fever
• severe headache • pain behind the eyes • joint and muscle pain • rash • nausea/vomiting • hemorrhagic (bleeding) manifestations |
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Dengue fever
Treatment |
• Usually mild
• No vaccine available • Symptomatic treatment (reduce fever) |
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Yellow Fever
Symptoms |
– Disease can range from mild to severe
– Most common form may be only fever and slight headache lasting a day or two – Severe disease characterized by high fever, nausea, nose bleeds and bleeding into the skin, “black vomit” from GI bleeding and jaundice – Mortality rate of severe disease can reach 50% – Reason for the variation in symptoms is unknown |
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Yellow Fever
Causative Agent |
– Enveloped, single-stranded RNA arbovirus
• Belongs to flavivirus family – Virus multiplies in mosquitoes • Mosquitoes transmit virus to humans |
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Yellow Fever
Pathogenesis |
– Introduce via bite of Aedes mosquitoes
– Multiplies and enters blood stream • Carried to liver – Jaundice results in liver damage – Injury to small blood vessels produces petechiae – Kidney failure is a common consequence of disease |
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Yellow Fever
Epidemiology |
– Reservoir mainly infected mosquitoes and primates in tropical regions of Central and South America and Africa
– Periodically spread to urban areas via mosquito bite |
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Yellow Fever
Prevention and Treatment |
– Control achieved by spraying and elimination of breeding sites
• Control almost impossible in jungle regions – Attenuated vaccine available for high risk groups – No proven antiviral treatment |
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Chikungunya
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• Enveloped, single-stranded RNA arbovirus, alpha virus (Togaviradae)
• Primary vector is Aedes aegypti, an aggressive daytime biter attracted to humans, and Aedes albopictus |
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Chikungunya
Symptoms |
• fever, • headache, • fatigue,
• nausea and vomiting, • muscle pain, • rash, • and joint pain. |
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African Sleeping Sickness
Symptoms |
– First symptoms appear within a week after bite from tsetse fly
• Nodule develops at site of bite • Regional lymph nodes enlarge – Symptoms may disappear spontaneously – Weeks or years later recurrent fevers develop – CNS involvement marked by gradual loss of interest in everything • Marked by decreased activity and indifference to food – Eyelids droop and individual falls asleep during everyday tasks – Speech becomes slurred followed by coma and death |
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African Sleeping Sickness
Causative agent |
– Trypanosoma brucei
• Flagellated protozoan • Slender with wavy undulating membrane • Two subspecies – T. brucei rhodesiense » Occurs mainly in cattle-raising areas of East Africa – T. brucei gambiense » Occurs mainly in forested areas of Central and West Africa • Transmitted by tsetse fly |
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African Sleeping Sickness
Pathogenesis |
– Protozoan enters through bite in fly saliva
– Organism multiplies at skin and migrates to lymphatic and blood circulation • Body responds with fever and IgM antibody – Symptoms improve – Period followed by recurrent increases in numbers of parasite • Termed parasitemica – Parasitemia and antibody production continue until treatment or death – T. brucei rhodesiense infections progress quickly often with major system involvement with 6 weeks and death in 6 months – T. brucei gambiense infections progress much more slowly |
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African Sleeping Sickness
Epidemiology |
– Disease occurs on African continent within 15° of equator
– 10,000 to 20,000 new cases annually – Occurrence of disease is determined by distribution of tsetse fly – Wild animals main reservoir for Rhodesian form – Humans are main reservoir for Gambian form • Human-to-human transmission more common |
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Malaria
Symptoms |
– “flu-like”
– Includes fever, headache and pain in the joints and muscles – Generally begin 2 weeks post infection • Transmission via bite of infected mosquito – Symptom pattern changes after 2 to 3 weeks • Falls into three categories – Cold phase – abruptly feels cold and develops shaking – Hot phase – follows cold phase » Temperature rises steeply reaching 104°F – Wet phase – follows hot phase » Temperature falls and drenching sweat occurs |
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Malaria
Causative agent |
– Human malaria caused by four species of genus Plasmodium
• P. vivax, P. falciparum, P. malatiae, P. ovale – Infectious form of parasite injected via mosquito – Carried by bloodstream to liver • Infects cells of liver – Thousands of offspring released to produce infection in erythrocytes |
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Malaria
Pathogenesis |
– Characteristic feature
• Recurrent bouts of fever followed by times of wellness – Caused by erythrocytic cycle of growth and release of offspring – Each species has different incubation periods, degrees of severity and preferred host age and range – Spleen enlarges to cope with large amount of foreign material and abnormal RBC • Common cause of splenic rupture – Parasites cause anemia by destroying red RBC and converting iron from hemoglobin to non-usable form – Stimulates immune system • Overworked immune system fails and immunodeficiency develops |
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Malaria
Epidemiology |
– Once common in both temperate and tropical areas
• Now dominantly disease of warm climate – Eliminated from continental U.S. in late 1940’s – Mosquitoes of genus Anopheles are biological vectors – Infected mosquitoes and humans constitute reservoir – Transmission via mosquitoes, blood transfusion and sharing of syringes |
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Malaria
Prevention and Treatment |
– Treatment is complicated
– Chloroquine • Effective against erythrocyte stage. Will not cure liver infection – Primaquine and tafenoquine • Generally effective against exoerythrocyte stage and certain species gametocytes |
