ID

Question 0

Pathologic mech of Anaplasmosis

Answer 0

Infects: marrow (myeloid & lymphoid progenitors) => liver, spleen, & lung pathology
Subversion of host response = cause of Sxs
* increased neutrophil & chemokine activity, & INF-g secretion

Question 1

Anaplasmosis clinical presentation

Answer 1

intercellular pathogen carried by Ixodes tick,
Sx: fever, chills, myalgias, headache, & anorexia (very non-specific)
Dx: wright or giemsa stained blood smear, or PCR, IFA
Tx: doxycycline or rifampin

Question 2

Characteristics of Babesia on blood smear

Answer 2

intraerthrocytic, pleiomorphic inclusions with TETRAD; not pigmented, may or may not be vacuolated.

Question 3

Babesiosis

Answer 3

obligate parasite, transmitted from mice by Ixodes tick;
cause erythrocyte rupture => normocytic hemolytic anemia.
3 possible Syndromes:
1. asymptomatic; 2. Mild-moderate malaise/fatigue
3. Severe: 20% mortality (DIC, splenic infarct…) *IF low cell immunity

Question 4

Treatment for Babesiosis

Answer 4

#1 (for mild-moderate illness): Atovaquone & azithromycin
2. Clindamycin & quinine IF severe.

Question 5

Rocky Mountain Spotted Fever

Answer 5

Rickettsia bacteria, incubation: 2-14 days.
Sx: abrupt onset fever, myalgias, + rash 2-5 days after onset (starts on wrists & ankles, spreads to trunk)
Tx: doxycycline (alternatively chloramphenicol if pregnant)

Question 6

Pathophysiology of Rickettsia infection

Answer 6

spread from skin via vasculature by OmpA & B proteins
=> phagocytosis by endothelial cells –> over-taken by bacteria (including cell’s actin filaments)
*

Question 7

P. falciparum malaria

Answer 7

Sx: fevers, malaise, chills & rigors (falciparum = most severe)
Incubation: 8-25 days;
Dx: thick and thin blood smear -> ring forms (esp. double), gametophytes and basophilic stippling
*sticky knobs => adherence to endothelium (evade clearance)
Complications: cerebral malaria! anemia, nephrotic syndrome

Question 8

“colonization resistance”

Answer 8

protection against infection BY presence of normal flora
(10^11 or 12 organisms in gut = normal!)
*compromised by antimicrobials
=> increased risk superinfection (C.diff, yeast, etc) if compromised

Question 9

Neutropenia as host defect

Answer 9

= INNATE host defense defect.
*usually not until VERY low granulocyte levels (<1,000)
Causative organisms: usually normal flora, esp initially;
(later on, = more obscure organisms)

Question 10

Effect of steroids on immune defenses

Answer 10

=> impaired CELL-mediated immunity

a host defense defect

Question 11

Viruses associated with impaired cell-mediated immunity

Answer 11

1. adenovirus
2. parainfluenza
3. CMV
4. HSV
5. herpes

Question 12

Bacteria associated with cell-mediated host defense defects

Answer 12

(6)

Listeria, legionella, TB, nocardia, shigella, salmonella

Question 13

Fungi associated with cell-mediated host defense defects

Answer 13

(4)

histoplasma, pneumocystis j, coccidioides, cryptococcus

Question 14

protozoans and helminthes associated with cell-mediated host defense defects

Answer 14

(4)

cryptosporidium, Leishmania, toxoplasma, strongyloides

Question 15

Common causes of impaired ADAPTIVE immunity

Answer 15

1. Asplenia OR complement deficiency
2. Malnutrition
3. Hyperglycemia
4. EtOH abuse
5. Antibody deficiencies (congenital OR secondary)

Question 16

IRIS (Immune Reconstitution Inflammatory Syndrome)

Answer 16

pathological inflammatory immunological response to (masked) opportunistic pathogens
CAN be fatal.
* Higher risk if RAPIDLY reduced viral loads (ie: young adults)