L29- Blood and Lymph Pathology II Flashcards
Filariasis is caused by (1) via (2) transmission, commonly in (3) geographical areas.
1- microfilarial nematode (thin, filamentous)
2- arthropod vectors (black flies, mosquitoes)
3- tropical disease, worse in Africa and Brasil, all N. American cases are imported
In filariasis, parasites enter the body to interfere with (1) function and cause (2) type damage in their associated organ. It is known to cause (3) specifically.
1- lymphatic function
2- inflammation => damage
3- elephantiasis
list the types of filariasis
Lymphatic: Wuchereria bancrofti, Brugia malayi, Brugia timori
Subcutaneous: Loa loa, Onchocerca volvulus
Serous cavity: Mansonella spp.
W. bancrofti is transmitted via (1) and infects humans in the (2) form. (2) form will travel to (3) in humans to develop into (4) and return to (5) in order to start producing (6). (1) will ingest (5) and (6) during feeding and allow (6) to develop back into (2) to prepare for another infection.
1- mosquitoes 2- L3 stage filarial larva 3- lymphatics 4- adult males/females worms 5- blood / lymph 6- sheathed microfilariae
Lymphatic Filariasis has (1) as the main clinical feature and (2) as the main sign in blood.
Other clinical features:
-(3) can occur in people with improper function lymph systems
-(4) are common feature affecting skin appearance
-(5) can occur in men
-(6) can occur in Asia
1- asymptomatic
2- microfilariae
3- lymphangitis, lymphadenitis, febrile illness
4- bacterial / fungal infections –> hardening/thickening of skin –> elephantiasis
5- hydrocele
6- lung infection (pulmonary tropical eosinophila syndrome): cough, wheezing, fever, eosinophilia
Lymphatic filariasis infections are usually acquired during (1) age. Subclinical lymphatic damage may be noted on (2). (3) is the most important clinical sign to noted in these patients. There is also an increased risk for (4). Overall, repeated (3) episodes and (4) may be superimposed to cause the conversion of (5) in lymphatic filarasis to (6).
1- childhood
2- lymphoscintigraphy, US
3- filarial fevers: acute inflammatory episodes
4- recurrent acute bacterial infections (due to fungal infection, cuts, scrapes, poor hygiene)
5- lymphedema
6- elephantiasis
Filariasis Dx
Conventional: thick blood film and membrane filter concentration (filter blood to concentrate parasites on slide)
Recent: IFA, ELISA, PCR / DNA probes, US, lymphoscintigraph
Filariasis Tx and prevention
Tx:
- anti-filarials
- surgery for hydrocele
- antibacterial / antifungal Tx for elephantiasis
Control: avoid mosquitoes via personal protection + community level vector control
Most tick-borne diseases harbor _____ type infections
- bacterial
- viral and protozoa are present, but rarer
Babesiosis is caused by (1), which is (non-/motile) and is transmitted via (3). (4) is the main species found in NE and Midwest US. The main reservoirs are (5).
1- Babesia spp., protozoa (parasite) 2- non-motile 3- deer tick 4- Babesia microti 5- dogs, deer, cattle, goat, sheep, horses, rodents (humans are accidental, dead end hosts)
Babesia microti:
- (1) are the definitive hosts that spread it, and is found in the (2) forms
- (1)/(2) will infect (3), the main reservoir, where (2) will feed on (4) and then produce (5)
- (6) part of (5) can infect (1) upon its blood meal and form (2) inside (1)
1- deer ticks
2- sporozoites
3- rodents (or other hosts- note humans are dead end hosts)
4- erythrocytes
5- (reproduce asexually) –> trophozoites, merozoites
6- merozoites –> male/female gametes [taken by (1) and converted into (2)]
Babesiosis clinical features:
- symptoms are mostly described as (1)
- (2) incubation period
- (3) patients may develop life-threatening disease
1- non-specific, mild-to-moderate viral-like illness that is self-resolving
2- 1-4 wks
3- asplenic Pts, immuno-compromised, organ damage/failure, elderly
Babesiosis clinical features:
list the possible complications
- low/unstable BP
- severe hemolytic anemia
- thromboytopenia
- DIC, or consumptive coagulopathy
- organ failure / damage
- death
Babesiosis Dx:
- (1) is the technique, indicate why it maybe misdiagnosed
- (2) describe Babesia appearance
- (3) is necessary for confirmation of Dx
1- blood smears: often misdiagnosed as malaria –> RBCs will appear similar
2- Babesia microti appears w/in RBCs as pear-shape / elliptical form (rarely as tetrad / maltese cross)
3- IFA (at CDC lab)
Babesiosis Tx and prevention
Tx: antibiotics, quinine
Control: avoid ticks and skin exposure, insect repellents, full-body exams, removal of ticks from clothes / pets
describe Plasmodium and list the relevant species
(for malaria)
-non-motile protozoa
-P. malariae, P. falciparum, P. vivax, P. ovale
plasmodium / malaria is spread via…..
Female Anopheles mosquito
Malaria will present with (1) symptoms and (2) as its hallmark feature. (3) will occur as a result of protozoal feeding which will eventually lead to (4).
1- (flu-like sxs) fever, HA, muscle pain, nausea
2- periodic cycles of chills, high fever, rigors/cold feeling (paroxysms) every 48-72 hrs
3- RBC lysis
4- splenomegaly
describe Sxs of malaria on day 1
1) COLD: dry skin, pale, cold, rapid pulse, low volume (1 hr)
2) HOT: high fever, full rapid-bounding pulse (2-6 hrs)
3) sweating (2-4 hrs, as fever declines)
(1) species of plasmodium are related to Benign tertian, where (2) is the more prevalent species of (1). (1) will usually infect and feed on (3). (1) are able to produce this effect because of (4) property, which occurs every (5- time)
(dormant in liver- allows for periodic symptoms)
1- P. vivax, P ovale
2- P. vivax
3- immature RBCs (as opposed to mature RBCs)
4- hypnozoite reforms and lies latent in liver
5- 48 hrs
P. malariae causes (1) malaria and infects (2). Although (3) is unable to occur, (1) occurs and is described as (4).
1- Quartan malaria
2- mature RBCs
3- relapse after eradication (no hypozoites form)
4- 72hr cycl`e paroxysms
P. falciparum causes (1) malaria and infects (2). (1) is characterized by (3).
-(4) are serious complications that can develop + (5) in the brain and (6) in the kidney
1- malignant tertian malaria
2- immature and mature RBCs
3- daily cycles of fever, sweating, shaking chills
4- severe hemolytic anemia, shock
5- blocks cerebral blood flow => coma, death (cerebral malaria)
6- (damage = ‘Blackwater fever) darkened urine
Malaria Dx:
- (1) species are clinically difficult to diagnose
- Dx in non-endemic areas requires (2) signs / components
- Dx in endemic areas requires (3) signs / components
- (4) list the direct diagnostic testing
1- P. vivax, P. falciparum
2- fever, anemia, hepatosplenomegaly (+ travel)
3- age, transmission patterns
4:
- Molecular: PCR, detects parasitic nucleic acids
- Rapid Tests: IFA, ELSA (parasitic Ag)
- **blood smear: contains parasites (GOLD standard)
- thick/thin smears
(1) is the gold standard test for malaria diagnosis. Blood samples are taken at (2) point and prepared in (3) and (4) fashion with (5) stains.
1- blood smear
2- between paroxysms episodes
3- thick film: assessment of more infected RBCs, more sensitive
4- thin film: single RBC visualization to identify internal features (ring forms, gametocytes)
5- Giemsa, Wright’s stains
list the P. falciparum complications:
- (1) kidney
- (2) liver
- (3) lungs
- (4) GIT
- (5) brain, + mortality rate and results in children
1- ARF
2- jaundice, fever
3- pulmonary edema
4- v/d
5- cerebral malaria: delirium –> coma –> death
- 20% case fatality in this complication
- 10% of children that survive cerebral malaria => long-term neuro-psychological deficits
Malaria:
- (inc/dec) incidences in pregnant women because of (2)
- (3) are the possible complications in mother, and fetus- due to (4)
1- increase
2- mosquitoes are more attracted to pregnant women
3- maternal mortality, abortion, still birth, premature delivery, low birthweight
4- vertical transmission
list the natural genetic protections against malaria and include the 1 acquired immunity
Genetic:
- SCD, α/β-thalassemia, G6PD deficiency
- hemolytic anemia
- Duffy Ag mutation
Acquired: repeated malarial infections => semi-immunity / partial immunity => absence of typical malarial symptoms