Steinhauer Flashcards
P. falciparum
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
P. vivax
Tropics but not that much in africa 10,000 merozoites per hepatic cycle Like reticulocytes Can relapse See schizont and macrogametocytes One ring
P. malariae
Cosmopolitan but spotty
Like older RBC
P. ovale
Can relapse
Likes young
P. knowlsi
Southeast asia
Anopheles
Face down, ass up, thats the way it likes to suck
Plasmodium life cycle
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
Ring troph
Signet ring trophozoite
Hemozoin with schizont
Can reenter cycle or make micro/macrogametocyte which get picked up by mesquito
How long until you have malaria symptoms
14-35 days
Uncompliccated malaria
Acute fever Paroxysms- chill then sweats Vivax every 48 hours benign tertian Falciparum every 72 hours malignant tertian Due to TNF-a Anemia
Complicated malaria
Organ failure
Cerebral- Neuro problems
Blackwater fever- Dark hemoglobinuria
Hyperparasittemia with 5% RBC infected
Why is P. falciparum more pathogenic
More merozoites, more invasion of RBC
PfEMP1- expression causes cytoadhesions=endothelium adhesions and rosetting and protects parasites from being cleared by spleen
Sticky cells and disease
TNF—iNOS which disrupts neurons- cerebral effects
Malarial relapse
Normally within 3-5 years
Have a dormant state in liver with clearance from RBC
P. vivax and ovale
Recrudescense
Low level in RBC with no hypnozoites
P. Falciparum
Plasmodium dx
Thick blood smear- recognize parasite
Thin blood smear- specific dx
Serological, PCR
Rapid- for falciparum (HRP2) and vivax
Genetic resistance to malaria
Sickle cell (PfEMP1 malformation, microRNA also disrupt parasite, and heme oxygenase 1 inhibits cerebral malaria)
Duffy blood groups (vivax and knowlesi)
Thalassemia
G6PDH
Duffy blood group
Genes common in africa, the reason why vivax doesn’t exist there
Lack of receptors for parasite attachment
Host defense of plasmodium
Spleen clears infected cells
Ab- Premunition: asymptomatic parasitemia (not common with travelers)
Babesia microti
Northeastern and upper midwest
Babesia divergens
Midwest and europe
Babesio duncani
West coast
Babesiosis general
Flu like symptoms unless immunocomprimised
Most via tick (Ixode scapularis and pacificus), some from blood transfusion
Important host- Permyscu leucopis mouse, same as Borrelia
Babesiosis life cycle
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.
Babesia microtilife cycle
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.
Babesia dx
No hemozoin (may not see with falciparum)
Ring form can make tetrad/ maltese cross
Can have multiple rings per cell
Irregular circles
Pathogenesis of Babesia
Serologic testing IFA (ELIZA for B. microti) Tick- 1-6 wks incubation Symptoms: Intermittent fever, dark urine 1-20% RBC normally infected Summer transmission
Erlichiosis chaffeensis
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)
Anaplasmosis phagocytophilum
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
Erlichiosis symptoms
1 wk incubation
fever, chlls, headache, myalgia, malaise
Ambylomma americanum tick vector
Anaplasmosis
1-2 week incubation
fever, chlls, headache, myalgia, malaise
Ixode vector
Ixode vector pathogens
Babesia, anaplasma, and borrelia burgdorferi
How to treat Ehrlichiosis, anaplasmosis, and early stage lyme disease
Doxycycline
Babesia tx
Clinda and quinine
Dermocentor vector pathogen
Erlichia, Ricketsia, Tularemia
Soft tick vector
Borrellia recurrentis
Herpes replication
Linear DNA, circular during infection
Rolling circle replication
EBV
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)
Mono
Pharyngitis
Hepatosplenomegaly (3-4 weeks)
Lyphadenopathy
atypical lymphocytes
CMV
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
Ampicillin rash
Caused when heterophile Abs are present
EBV
HIV
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
HIV testing
1/2nd gen- IgG test
3rd gen- IgM test
4th- Can test for IgM or Ag
Pneumocystis pneumonia
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
Candidiasis
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
Atypical mycobacterioses
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
Cryptococcosis
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
