Infections of the Circulatory, RES & Lympahtics-Parasitic Flashcards
Agent of African Trypanosomiasis
T. brucci
Agent of Chagas’ Disease
T. cruzi
Leishmaniasis agent
Leishmania sp.
Malaria agent
Plasmodium sp.
Babesiosis agent
Babesia sp.
T. brucci (African Trypanosomiasis) vector
Tsetse flies
T. cruzi (Chagas’ Disease) vector
Reduvid Bugs
Leishmania sp. (Leishmaniasis) vector
Sandflies
Plasmodium sp. (Malaria) vector
Mosquitoes
Babesia sp. (Babesiosis) vector
Ticks
Sleeping sickness (African Trypanosomiasis) is caused by
Trypanosoma brucei
causes wasting disease in cattle called “Nagana”
Trypanosoma brucei
causes west african sleeping sickness (human to human)
T. brucei gambiense
causes east african sleeping sickness (human to human, animal to human)
T. brucei rhodesiense
Early stage of African Trypanosomiasis infection
organisms in blood and peripheral lymph nodes, also fever, myalgia, chills, lymph node swelling (West)
Late stage of African Trypanosomiasis infection
Invasion of CNS, headache, seizures, tremors, encephalitis, periods of sleeplessness and lethargy, coma and death
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
Dx: African Trypanosomiasis
detection of parasites in blood smear, lymph node aspirate, or CSF
Control of African Trypanosomiasis
control tsetse fly populations
African Trypanosomiasis is the classical example of this immune defense
Antigenic variation
Tx of African Sleeping Sickness
melarsoprol (80% effective, but 5% or more develop encephalopathy due to drug-replaced now by DFMO)
difluoromethylornithine (DFMO)
First signs of Chagras’ disease
fever, local swelling, periorbital edema, myocarditis myalgia, malaise, hepatosplenomegaly
Once in the human host Trypanosoma cruzi takes on this form which spread systemically over many years
amastigote
Chronic Chagras’ disease- due to infection of cardiac muscle and myenteric plexus
dysrhythmias, cardiomyopathy, megaesophagus, megacolon (death from heart attack)
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