Steinhauer Flashcards

1
Q

P. falciparum

A

Mostly tropics
30,000 merozoites from hepatic cycle
Like younger cells
Only see multiple ring form and gametocytes (banana shaped)
Only one to do the clumping and rosetting

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2
Q

P. vivax

A
Tropics but not that much in africa
10,000 merozoites per hepatic cycle
Like reticulocytes
Can relapse
See schizont and macrogametocytes
One ring
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3
Q

P. malariae

A

Cosmopolitan but spotty

Like older RBC

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4
Q

P. ovale

A

Can relapse

Likes young

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5
Q

P. knowlsi

A

Southeast asia

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6
Q

Anopheles

A

Face down, ass up, thats the way it likes to suck

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7
Q

Plasmodium life cycle

A

Mesquito injects sporozoits into human
Make it to liver by inducing parasitophorous vacuole
The replicate and release merozoites back into blood
Make it to blood cells and make trophozoites

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8
Q

Ring troph

A

Signet ring trophozoite
Hemozoin with schizont
Can reenter cycle or make micro/macrogametocyte which get picked up by mesquito

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9
Q

How long until you have malaria symptoms

A

14-35 days

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10
Q

Uncompliccated malaria

A
Acute fever
Paroxysms- chill then sweats
Vivax every 48 hours benign tertian
Falciparum every 72 hours malignant tertian
Due to TNF-a
Anemia
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11
Q

Complicated malaria

A

Organ failure
Cerebral- Neuro problems
Blackwater fever- Dark hemoglobinuria
Hyperparasittemia with 5% RBC infected

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12
Q

Why is P. falciparum more pathogenic

A

More merozoites, more invasion of RBC
PfEMP1- expression causes cytoadhesions=endothelium adhesions and rosetting and protects parasites from being cleared by spleen

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13
Q

Sticky cells and disease

A

TNF—iNOS which disrupts neurons- cerebral effects

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14
Q

Malarial relapse

A

Normally within 3-5 years
Have a dormant state in liver with clearance from RBC
P. vivax and ovale

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15
Q

Recrudescense

A

Low level in RBC with no hypnozoites

P. Falciparum

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16
Q

Plasmodium dx

A

Thick blood smear- recognize parasite
Thin blood smear- specific dx
Serological, PCR
Rapid- for falciparum (HRP2) and vivax

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17
Q

Genetic resistance to malaria

A

Sickle cell (PfEMP1 malformation, microRNA also disrupt parasite, and heme oxygenase 1 inhibits cerebral malaria)
Duffy blood groups (vivax and knowlesi)
Thalassemia
G6PDH

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18
Q

Duffy blood group

A

Genes common in africa, the reason why vivax doesn’t exist there
Lack of receptors for parasite attachment

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19
Q

Host defense of plasmodium

A

Spleen clears infected cells

Ab- Premunition: asymptomatic parasitemia (not common with travelers)

20
Q

Babesia microti

A

Northeastern and upper midwest

21
Q

Babesia divergens

A

Midwest and europe

22
Q

Babesio duncani

A

West coast

23
Q

Babesiosis general

A

Flu like symptoms unless immunocomprimised
Most via tick (Ixode scapularis and pacificus), some from blood transfusion
Important host- Permyscu leucopis mouse, same as Borrelia

24
Q

Babesiosis life cycle

A

After feeding, adult females drop off the third host to lay eggs(1), usually in the fall. Eggs hatch into six-legged larvae(2)and overwinter in the larval stage. In the spring, the larvae seek out and attach to the first host, usually a small rodent(3). Later in the summer, engorged larvae leave the first host(4)and molt into nymphs(5), usually in the fall. The ticks overwinter in this stage. During the following spring, the nymphs seek out and attach to the second host(6), usually another rodent (e.g., a mouse) or lagomorph (e.g., a rabbit). The nymphs feed on the second host and drop off later in the summer(7). Nymphs molt into adults(7a-7b)off the host in the late summer or fall, and overwinter in this stage. The next spring, adults seek out and attach to a third host, which is usually a larger herbivore (including cervids and bovids), carnivore, or human(8). The adults feed and mate on the third host during the summer. Females drop off the host in the fall to continue the cycle. Females may reattach and feed multiple times. The three hosts do not necessarily have to be different species, or even different individuals. Humans may serve as first, second or third hosts.

25
Q

Babesia microtilife cycle

A

TheBabesia microtilife cycle involves two hosts, which includes a rodent, primarily the white-footed mouse,Peromyscus leucopus,and a tick in the genus,Ixodes. During a blood meal, aBabesia-infected tick introduces sporozoites into the mouse host. Sporozoites enter erythrocytes and undergo asexual reproduction (budding). In the blood, some parasites differentiate into male and female gametes although these cannot be distinguished at the light microscope level. The definitive host is the tick. Once ingested by an appropriate tick, gametes unite and undergo a sporogonic cycle resulting in sporozoites. Transovarial transmission (also known as vertical, or hereditary, transmission) has been documented for “large”Babesiaspp. but not for the “small” babesiae, such asB. microti.
Humans enter the cycle when bitten by infected ticks. During a blood meal, aBabesia-infected tick introduces sporozoites into the human host. Sporozoites enter erythrocytesand undergo asexual replication (budding). Multiplication of the blood stage parasites is responsible for the clinical manifestations of the disease. Humans are, for all practical purposes, dead-end hosts and there is probably little, if any, subsequent transmission that occurs from ticks feeding on infected persons. However, human to human transmission is well recognized to occur through blood transfusions.

26
Q

Babesia dx

A

No hemozoin (may not see with falciparum)
Ring form can make tetrad/ maltese cross
Can have multiple rings per cell
Irregular circles

27
Q

Pathogenesis of Babesia

A
Serologic testing IFA (ELIZA for B. microti)
Tick- 1-6 wks incubation
Symptoms: Intermittent fever, dark urine
1-20% RBC normally infected
Summer transmission
28
Q

Erlichiosis chaffeensis

A
Rickettsial tick borne
Intracellular G-
Human monocytic ehlichiosis
Morula in monocyte
Amblyomma vector, deer reservoir
Gets worse with age
South midatlantic, north/south
Can get rash everywhere (also hands/feet)
29
Q

Anaplasmosis phagocytophilum

A
Rickettsial tick borne
Intracellular G-
Human granulocytic anaplasmosis
Morula in granulocytes
Ixodes scapularis and pacificus vector and white footed mouse reservoir
Mostly Eastern states, more north
Gets worse with age
30
Q

Erlichiosis symptoms

A

1 wk incubation
fever, chlls, headache, myalgia, malaise
Ambylomma americanum tick vector

31
Q

Anaplasmosis

A

1-2 week incubation
fever, chlls, headache, myalgia, malaise
Ixode vector

32
Q

Ixode vector pathogens

A

Babesia, anaplasma, and borrelia burgdorferi

33
Q

How to treat Ehrlichiosis, anaplasmosis, and early stage lyme disease

A

Doxycycline

34
Q

Babesia tx

A

Clinda and quinine

35
Q

Dermocentor vector pathogen

A

Erlichia, Ricketsia, Tularemia

36
Q

Soft tick vector

A

Borrellia recurrentis

37
Q

Herpes replication

A

Linear DNA, circular during infection

Rolling circle replication

38
Q

EBV

A
Mono with heterophiles
Nasopharyngial carcinoma
Burkitt’s lymphoma (Higher if with malaria)
Hodgkin lymphoma
Gastric carcinoma
Kissing disease
CR2 (a/k/a CD21), on susceptible cells
Activates B cells= LN swelling
Activates CTLs (atipical lymphocytes)
39
Q

Mono

A

Pharyngitis
Hepatosplenomegaly (3-4 weeks)
Lyphadenopathy
atypical lymphocytes

40
Q

CMV

A
Mono 
Pneumonia
Retinitis, esophagitis in immunocompremised
Monospot negative
Owl eye in histology
Exudate tonsillitis more rare!!!
Dx: Histo and PCR 

Evade CD8 cells by inhibiting MHC1 expression

41
Q

Ampicillin rash

A

Caused when heterophile Abs are present

EBV

42
Q

HIV

A
GALT important
Symptoms like MONO
Thrush and rash as well
\+ssRNA diploid  with env
LTR- 5' RNA transcript, 3' term/poly/int
gp120 (adhere) gp41(fusion) ENV
Gag, Pro, Pol, Env
2-4 weeks for symptoms
43
Q

HIV testing

A

1/2nd gen- IgG test
3rd gen- IgM test
4th- Can test for IgM or Ag

44
Q

Pneumocystis pneumonia

A
Dry cough, low fever, dyspnea with hypoxia
Butterfly chest xray (bilateral interstitial)
Elevated LDH (over 500mg/dl)
Consider CMV and pneumococci
Do Bronchoaveolar lavage (BAL) to rule these out.
Stain + with silver
Monitor kidney function with tx
DDx-Streptococcal pneumonia
Tuberculosis
Disseminated MAC
Tx- TMP-SMZ for 21 days
Steroids for airway inflammation control
45
Q

Candidiasis

A

Taste disturbance, sometimes burning
Erythematous mucosa
C. Esophagitis- dysphagia, retrosternal pain, nauseau
Do not confuse with Oral Hairy Leukoplakia (OHL) related to EBV
Consider Alcoholism and steroid tx

Tx- Oral 7 days, esophageal 14-21 days of fluconazole

46
Q

Atypical mycobacterioses

A
MAC (M Avium)
Elevated Alk. Phos
Try to culture sputum
Bone marrow/lymph for confirmation
CD4 <50, use prophylaxis to prevent dissem.
Diss.- Multi organ, liver more common
DDx- TB or malignant lymphoma

preferred: clarithromycin + ethambutol
alternative to clarithromycin: azithromycin
Use for more than 12 months

47
Q

Cryptococcosis

A
Southeast asia, and US
Neuro problems with increased ICP, do LP
Atipical pneumonia/ chest pain/unproductive cough
Photophobia and low grade fever
Extensive abscesses
Lesions resemble molluscum cantagiosum
Tx- Amphotericin B and flucytosine (induction phase) monitor renal fx
Fluconazole (consolidation phase) 400mg
Fluconazole 200mg (maintenance)

+ for india ink, antigen good for Dx