L30- Multi-system Infections II Flashcards
list the common vector-borne diseases carried by the following:
- (1) mosquito
- (2) tick
- (3) fly
1- YF, Dengue, Zika, ChikV
2- *Lyme disease, *Rocky Mountain Spotted fever; Ehrlichiosis, Anaplasmosis
3- Leishmaniasis, Trypanosomiasis (american, african)
Rocky Mountain Spotted fever is caused by (1) pathogen
Lyme disease is caused by (2) pathogen
1- rickettsia rickettsii
2- borrelia burgdorferi
rickettsia rickettsii is carried by (1) tick
borrelia burgoferi is carried by (2) tick
1- Dermacentor spp.
2- Ixoides spp.
Lyme Disease:
- (1) pathogen
- (2) associated tick, common name
- (3) incubation period
- (4) duration
- (5) rash description
- (6) main common symptoms
1- borrelia burgdorferi 2- black-legged tick, deer tick 3- 3-30 days 4- wks 5- bull's eye rash 6- fever, arthralgia, myalgia
Rocky Mountain Spotted fever:
- (1) pathogen
- (2) associated tick, common name
- (3) incubation period
- (4) duration
- (5) rash description
- (6) main common symptoms
1- rickettsia rickettsii 2- Rocky Mountain wood, American dog, brown dog 3- 2-14 days 4- wks 5- macular / petechiae rash 6- fever, arthralgia, myalgia
Rickettsia rickettsii: list the many important bacterial features
- small obligate intracellular Gram- rod
- non-motile, pleomorphic (shape)
Rickettsia rickettsii:
- (1) critical geographic areas
- (2) critical season
- (3) are the other risk factors
1- NC, SC, OK, TN
2- Apr. – Sept. (late spring thru summer)
3- dog exposure, residence near forest / tall grass, children (5-9 y/o), males
Once ricketsia rickettsii is inoculated into skin, pathogens will travel to (1) cells via (2) and then multiply via (3) process. (4) is the mechanism of the rash and petechial lesions, plus is the basis for the other systemic symptoms. (5) is the typical immune response.
1- endothelium and vascular smooth muscle cells
2- blood
3- binary fission in cytoplasm –> damage heavily parasitized cells
4- RBC’s leak thru breaks in BVs (same process in other organs)
5- T cell mediated: IFN-γ, TNF-α
Rickettsia rickettsii:
- (1) incubation period
- (2) initial presentation
- (3) subsequent Sxs- many
- (4) is the dangerous complication, indicate time period
1- 2-14 days
2- abrupt onset fever, HA
3- fever/chills, rash, HA, n/v/d, abdominal pain, myalgia, loss of appetite, photophobia, sometimes conjunctival injection
4- fatal in first 8 days if not treated correctly
describe the initial presentation and progression of rash in Rocky Mountain Spotted fever
Early: red to purple, spotted/petechial rash seen around day 5 of Sxs — starts peripherally (ankles, wrists)
Late: 35-60% of Pts, rash spreads proximally on limbs (more spotted)
(1) is the main complication / concern with rickettsia rickettsii infections. (2) is the immediate risk from (1) and (3) is the concern if (1) is severe early in the infection. If (1) does not occur, Rocky Mountain Spotted fever will take (4) for recovery.
1- vasculitis (damaged BVs) => clotting / bleeding
2- fluid loss –> loss of circulation to extremities –> digital necrosis –> amputation
3- permanent long-term health deficits (neurological or to other internal organs)
4- days to months
Rocky Mountain Spotted fever:
- (1) are the recommended technique for diagnosis
- (2) are the many other possible tests used
- (3) is used for disease confirmation
1- IFA (indirect immunofluorescent assay) and EIA (enzyme immunoassays)
2:
- serology: 4-fold change in Ab titers (paired samples)
- direct IFA
- skin biopsy
- Weil-Felix: IHC Ag detection
3: specialized PCR for serum Abs
Borrelia Burgdorferi:
- (1) describe important bacterial features
- (2) geographic predominance
- (3) season predominance
- (4) describe briefly process of tick bite that spreads disease
1- Gram- spirochete
2- NE USA, N Mid-west —- Pacific coast
3- late spring thru summer
4- must be attached for 36-48hrs (or from incorrect removal of tick –> head breaks and releases bacteria)
Borrelia Burgodorferi:
- infects hosts / vectors in (1) stage
- infects humans in (2) stage
- (3) is special characteristic of blacklegged ticks lifecycle
1- (not eggs) larva –> nymph –> adults
2- nymph –> adults
3- population can double w/in 2 yrs
In Lyme disease pathogenesis, borrelia burgodorferi produces (1) to mediate binding to (2). Then infection induces synthesis of (3), affecting local area of infection. The infection spreads via (4). (5) are the factors that help the Spirochete evade host immune response and be resistant to (6) killing.
1- adhesins
2- glycoaminoglycans (GAGs) and integrins
3- pro-and anti- inflammatory CKs
4- lymph –> regional lymphadenopathy –> distant tissues (wks/mos)
5- factor H proteins, Ag variation
6- complement mediated killing
list the common symptoms of Lyme disease, most to least prevalent
- EM: erythema migrans rash, 71%
- arthritis, 28%
- facial palsy (9%), radiculopathy (4%), meningitis/encephalitis (2%), carditis (1%)
Lyme disease:
- (1) incubation period
- (2) describe progression of rash (onset to disappearance)
- (3) describe the other symptoms and duration
1- 3-30 days (at bite site)
2- ECM = erythema chronicum migrans = slowly expanding red ring = bull’s eye rash (leading edge contains pathogen) —-> disappears w/in wks
3- fever, myalgia, arthralgia may last for months (meningeal irritation also)
Lyme disease: briefly describe initial / first stage of presentation (1/3, include timing)
(incubation, 3-30 days)
- ECM rash
- accompanied flu-like Sxs
- organism spreads via lymph / blood to MSK, skin, CNS, heart, etc
Lyme disease: briefly describe second stage of presentation (2/3, include timing)
wks - mos after onset
- arthritis / arthralgia
- cardiac complications
- neurological complications (meningitis, facial palsy)
Lyme disease: briefly describe third stage of presentation (3/3, include timing)
mos - yrs after onset
- starts with return of chronic arthritis
- progressive CNS disease
-rarely fatal, but poor quality of life w/o Tx
Lyme Disease treatment:
- (1) is common after course of treatment
- (2) describe PTLDS
1- lingering fatigue, pain, joint/muscle aches after 2-4 wks of Tx
2- post-treatment Lyme disease syndrome:
- small % of cases, Sxs lasting >6mos
- ‘chronic Lyme disease’
- cause is unknown
Lyme Disease Dx:
- (1) is recommended technique
- (2) are alternate techniques- include important drawback for one of them
- (3) is not recommended, explain
- (4) is used for confirmation
1- EIA (enzyme immuno-assay), IFA (immuno-fluorescence assay)
2- serology; nucleic acid PCR: can’t distinguish between DNA of dead or alive bacteria
3- Culture: 6-8 wks + low sensitivity
4- immunoblot assay via EIA
describe two-tiered Lyme disease testing
1st: EIA or IFA
2nd: IgM/IgG or IgG only Western blot
Leishmaniasis via (1) vector mainly refers to infection via (2) species causing (3) type leishmaniasis. (4) are the main geographic areas affected.
1- sand fly
2- L. donovani, L. infantum
3- visceral (not cutaneous or mucosal)
4- East Africa, India
indicate the important microbial features of leshmania spp.
- protozoal parasite: blood and tissue
- locomotion via flagella
Leishmaniasis spp.:
- (1) infectious form
- (2) diagnostic form
- (3) describe transition from (1) to (2)
1- promastigote
2- amastigote
3- loses flagellum
Visceral Leishmaniasis:
- (1) incubation period
- (2) three basic outcomes
(aka black fever, kala-azar fever)
1- wks to yrs
2:
i) self-limiting infection
ii) chronic debilitating process
iii) fulminating rapidly fatal disease
Visceral Leishmaniasis:
- (1) are the initial symptoms, resembling (2) presentation, aka a DDx
- then parasite invades (3) to cause (4) symptoms
- (5) maybe a complication of successful treatment
1- chills, undulant fever (T goes up / down)
2- malaria
3- RES (reticuloendothelial system)
4- hepatosplenomegaly, weight loss, anemia, emaciation
5- depigmented, granulomatous eruptions on skin –> post-kala-azar dermal leishmaniasis
(T/F) leishmaniasis and trypanosomiasis are considered HIV/AIDS opportunistic infections
F- only leishmaniasis
Leishmaniasis Dx:
- (1) is the best method
- (2) are alternate methods
1- microscopic identification
2- Abs for parasites; urine testing; PCR
American Trypanosomiasis (bonus- alternate name):
- (1) pathogen
- (2) arthropod vector
- (3) geographic areas
aka- Chaga’s disease
1- T. cruzi; protozoal parasite
2- Reduviid bug = ‘kissing bug’
3- Mexico, central and south america
describe the steps of T. cruzi infection /multiplicaiton starting from bug bite
1) painless bug bite from Reduviid bug
2) bug delivers feces to bite site
3) inoculation by rubbing bug feces into Conjunctiva, Bite site, or another break in Skin
4) multiplication in blood
5) dissemination
6) amplification in muscle, nerve fibers
T. cruzi:
- (1) infectious form
- (2) diagnostic form
- (3) describe transition from (1) to (2)
1- metacyclic trypomastigotes
2- amastigotes
3- loses flagellum
Following bite, T. cruzi in the (1) form will enter to infect (2) cells. (1) form is then transformed into (3) form allowing binary fission to occur. Daughter cells will them undergo (4) transformation and then (5) will occur in infected cell.
1- metacyclic trypomastigote
2- macrophages, fibroblasts, muscle tissue
3- amastigote (w/in host cells)
4- back to trypomastigotes
5- lysis of cell –> further dissemination of protozoa
list the phases of American Trypanosomiasis, include timeline
1) Acute phase- lasts 2 mos post infection
2a) Chronic indeterminate phase (prolonged asymptomatic phase)
2b) Chronic phase: life-threatening conditions
American Trypanosomiasis, acute phase:
- (1) duration
- (2) is the main clinical sign, explain
- most patients experience (3) type of infection
- (4) are the other features / Sxs
- (5) parasite status in blood
1- 2 mos post-infection
2- Romana’s sign: unilateral swelling of eyelid via rubbing eye with T. cruzi via bug feces
3- asymptomatic or mild/unspecified infection
4- fever, HA, lymphadenopathy, pallor, myalgia, dyspnea, swelling, chest/abdominal pain
5- high number found in circulation
American Trypanosomiasis, chronic phase:
most go into (1) chronic phase, with (2) as the status of parasite in blood
(3) % will go into chronic phase characterized by (4):
- (5) and (6) are the general disorders patients suffer
- (7) may occur in the later years of (4)
1- chronic indeterminant - asymptomatic phase
2- few to no parasites in circulation (IgGs seen)
3- 20-30%
4- life-threatening conditions
5- 30% with cardiac disorder
6- 10% with digestive, neurological, or mixed alterations
7- sudden death: arrhythmia, progressive HF, destruction of heart muscle or CNS
American Trypanosomiasis complications:
- (1) CVS
- (2) GIT
- (3) immuno-compromised Pts
1- arrhythmia –> sudden death (dilated heart not pumping well)
2- dilated esophagus or colon –> dysphagia or constipation (+ other issues)
3- maybe reactivated in AIDS or chemotherapy Pts => severe course of disease
describe the diagnosis of American Trypanosomiasis: samples, results
Microscopic identification:
-CSF via lumbar puncture, palpate swollen cervical LNs
-Large ‘C’ shaped protozoan in cells –> Kinetoplast near nucleus (= circular mitochondrial DNA near nucleus)
African Trypanosomiasis (bonus- alternate name):
- (1) pathogens (include reservoirs)
- (2) arthropod vector
- (3) geographic areas
(human African sleeping sickness)
1:
-trypanosoma brucei gambiense: human reservoirs (maybe domesticated animals)
-t.b. rhodesiense: animal reservoirs
2- Tsete fly
3- t.b.g. West Africa, t.b.r. East Africa
African Trypanosomiasis, T. brucei spp.:
- (1) infectious form
- (2) diagnostic form
- (3) site(s) of multiplication
1- metacyclic trypomastigote
2- trypomastigote
3- blood, lymph, CSF
African Trypanosomiasis, T. brucei spp., pathogenesis:
-1st stage: multiplication of pathogen occurs in (1) areas and (2) symptoms begin
-2nd stage: parasites travel to (3) causing (4) disturbances, where (5) is the hallmark feature –> (6) could be the possible end progression without treatment
1- blood, lymph, subcutaneous tissues
2- bouts of fever, HA, arthralgia, itching
3- across BBB –> CNS
4- behavioral changes, confusion, sensory disturbances, poor coordination
5- sleep-cycle disturbances
6- coma —> death
Trypanosoma brucei spp.:
-(1) which is more common, and is more in (East/West) Africa, and its infection progresses more (rapid/slow)
1- T.b. gambiense
2- West Africa
3- slow
T.b. rhodesiense: East Africa, rapid progression
T.b. rhodesiense:
-(1) incubation period for major Sxs to appear, generally including (2) and ending with (3)- includes its timeline
- (4) occurs at bite site in some patients
- (5) Sxs may appear 1-2 wks after bite
1- few wks - mos
2- CNS infection: mental deterioration + neurological problems (***sleep issues)
3- death w/in a few mos
4- large sore / chancre
5- fever, HA, myalgia, arthralgia, lymphadenopathy (maybe rash)
T.b. gambiense:
- (1) initial symptoms, include timeline
- (2) second phase of symptoms, include timeline
- (3) describe end-course progression
1- Wks-Mos: intermittent fevers, HA, myalgia, arthralgia, pruritus, lymphadenopathy, weight loss
2- 1-2yrs, CNS involvement:
- Mainly: *daytime sleepiness + nightime disturbances, personality changes, progressive confusion
- Possibly: partial paralysis, balance issues, hormonal imbalance
3:
- usually death w/in 3yrs
- rarely lasts longer than 6-7yrs
discuss diagnosis of African Trypanosomiasis
Microscopic Identification
-lumbar puncture for CSF sample and cervical LN palpation are also useful
