Infections of the Circulatory, RES & Lympahtics-Parasitic Flashcards by Kimberly Miller

Agent of African Trypanosomiasis

T. brucci

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Agent of Chagas’ Disease

T. cruzi

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Leishmaniasis agent

Leishmania sp.

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Malaria agent

Plasmodium sp.

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Babesiosis agent

Babesia sp.

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T. brucci (African Trypanosomiasis) vector

Tsetse flies

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T. cruzi (Chagas’ Disease) vector

Reduvid Bugs

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Leishmania sp. (Leishmaniasis) vector

Sandflies

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Plasmodium sp. (Malaria) vector

Mosquitoes

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Babesia sp. (Babesiosis) vector

Ticks

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Sleeping sickness (African Trypanosomiasis) is caused by

Trypanosoma brucei

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causes wasting disease in cattle called “Nagana”

Trypanosoma brucei

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causes west african sleeping sickness (human to human)

T. brucei gambiense

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causes east african sleeping sickness (human to human, animal to human)

T. brucei rhodesiense

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Early stage of African Trypanosomiasis infection

organisms in blood and peripheral lymph nodes, also fever, myalgia, chills, lymph node swelling (West)

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Late stage of African Trypanosomiasis infection

Invasion of CNS, headache, seizures, tremors, encephalitis, periods of sleeplessness and lethargy, coma and death

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This form of African Trypanosomiasis (sleeping sickness) has a longer incubation period of weekts to months and CNS involvement after weeks or years as opposed to the other form which develops both within a month

West African form

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Dx: African Trypanosomiasis

detection of parasites in blood smear, lymph node aspirate, or CSF

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Control of African Trypanosomiasis

control tsetse fly populations

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African Trypanosomiasis is the classical example of this immune defense

Antigenic variation

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Tx of African Sleeping Sickness

melarsoprol (80% effective, but 5% or more develop encephalopathy due to drug-replaced now by DFMO)
difluoromethylornithine (DFMO)

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First signs of Chagras’ disease

fever, local swelling, periorbital edema, myocarditis myalgia, malaise, hepatosplenomegaly

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Once in the human host Trypanosoma cruzi takes on this form which spread systemically over many years

amastigote

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Chronic Chagras’ disease- due to infection of cardiac muscle and myenteric plexus

dysrhythmias, cardiomyopathy, megaesophagus, megacolon (death from heart attack)

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Reduvid bugs pass Trypanosoma cruzi to humans by

through the feces left on the skin after biting the human

What is one resevoir for Chagras' disease in the lower US?

animal vectors (raccoons, opossums)

periorbital edema caused by Chagras' disease-first sign

Romana's sign

most individuals remain in this stage for life where there are few trypanosoma cruzi in the blood and a high level of Ab

Indeterminate (Asymptomatic phase)

What is the biggest difference between African and American Trypanosomiasis

African Trypanosomiasis is extracellular, American is intracellular

Dx: acute phase of American Trypanosomiasis

detection of parasites in peripheral blood

Dx: chronic disease

serology

has a single flagella

Leishmania spp.

intracellular in macrophages

Leishmania spp

transmitted by flies which pick up blood from an infected individual including infected macrophages and spreads it to another individual

Leishmania spp.

opportunistic pathogen in HIV + individuals, primarily in the mediterranean

Leishmaniasis

important resevoirs of Leishmaniasis

Canines, rodents

3 forms of Leishmaniasis

cutaneous, mucocutaneous, visceral

Visceral form of Leishmaniasis is caused by

L. donovani, L. infantum, L. chagasi

parasites are found in the reticuloendothelial system-macrophages of liver, spleen, bone marrow, etc

Leishmaniasis

full blown disease presents as fever, weight loss, hepato-splenomegaly, a "wasting" appearance, systemic immuno-suppression

Leishmaniasis-visceral

common cause of death is secondary bacterial and viral infection

Leishmaniasis visceral

Why do antibodies afford little or no protection against Leishmaniasis?

Leishmaniasis have only intracellular amastigotes-so antibodies won't work!

Tx: Leishmaniasis

gamma-interferon mediated activation of macrophages, heavy metal compounds (considerable toxicity)

Eliminated malaria from the US in 1940s using

DDT, draining swamps and wetlands, and screens for windows/air conditioning-reduced exposure tme

Why do competent vector mosquitoes in the US typically not spread malaria

there are few individuals to transmit it from, can happen if an infected traveler returns to the US

4 species of Plasmodium that cause malaria in humans

P. falciparum, P. vivax, P. malariae, P. ovale

Species that take on a form called a hypnozoite that can stay dormantin the liver for decades and then can cause malaria (common in vietnam vets)

P. vivax, P. ovale

characteristic clinical feature of malaria

malarial paroxysm-merozoites lysing RBCS when replicating, causes flu-like symptoms (fever, chills, headache, muscle ache)

flu-like patterns recur every 48 hrs

P. vivax, ovale

flu-like patterns recur every 72 hrs

P. malariae

flu-like patterns recur every 48 hrs

P. falciparum

malarial paroxysm stages

cold stage, hot stage, sweat stage

common complication of malaria

anemia

waste products of plasmodium replication can stimulate TNF-alpha, IL-1 and other cytokine release from the immune system causing

suppression of erythropoiesis

plasmodium infected RBCs are

destroyed by the spleen

highest number of RBC lysis in malaria is seen in infections with

P. falciparum (infects both mature and young erythrocytes)

can only infect older erythrocytes

plasmodium malariae

can only infect young RBCs (reticulocytes)

P vivax (Duffy +) P. ovale (Duffy -/+)

complication of malaria from consumption of glucose by plasmodium falciparum that causes lactic acidosis that may affect CNS function

hypoglycemia

RBC infected by P. falciparum get bumps on their surface and stick together blocking microvasculature in the brain

cerebral malaria

Dx: malaria

recognize clinical syndrome, travel history, blood smear positive for parasites

rodents and cattle serve as reservoirs

Babesia spp. (Babesiosis)

symptoms develop 1-8 weeks after bite: fever, chills, malgia, hemolytic anemia (many infections are asymptomatic-symptomatic more in elderly, asplenic, immunosuppressed)

Babesiosis

Tx: Babesiosis

atovaquone, azithromycin (quinine/clindamycin)

maltese cross in RBCs is a distinguishing characteristic of

Babesiosis

Wuchereria bancrofti and Brugia malayi cause

Filariasis (lymphatic filariasis)

Wuchereria bancrofti and Brugia malayi exert their effects by

infecting lymphatic vessels and obstructing flow causing elephantiasis

Filariasis is transmitted by

the bite of infected mosquitoes

high IgE, eosinophilia, asthma associated with filariasis

Tropical Pulmonary Eosinophilia

acute infection indicated by fever, chills, and lymphadenitis-painful swelling may last for weeks and recur frequently

Filariasis

Dx: Filariasis

observation of microfilariae in blood smears

Tx: Filariasis

microfilariae killed and adults damaged by DEC

used to counteract allergic response to dying worms in Filariasis

Steroids

Caused by schistosoma spp.

Schistosomiasis

snails are part of the life cycle

Schistosoma spp.

swimming in water contaminated with human sewage allows cercariae to penetrate the skin in this disease

Schistosomiasis

Are shed in both feces and urine due to migration of schistosomulae

Schistosoma eggs (Shistosomiasis)

inhabits venous plexus of the large intestine

Schistosoma mansoni

inhabits venous plexus of the small intestine

Schistosoma japonicum

inhabits the venous plexus of the bladder

Schistosoma haematobium

lodging of eggs causes inflammation and possible fibrosis/cirrhosis resulting in loss of bladder and liver function

Shcistosomiasis Chronic Infection

Dx: of Schistosomiasis

eggs in feces or urine

Control or prevention of Schistosomiasis

control snail population, limit exposure to water, improve sanitation

cause chronic intestinal and hepatic dysfunction-portal fibrosis and hypertension

S. japonicum and S. mansoni

causes hematuria, dysuria, urinary frequency, loss of bladder function, increased occurrence of squamous cell carcinoma of the bladder

S. haematobium