4 - 1 Vectorborne Flashcards

(60 cards)

1
Q
  1. Which mosquito genus is the primary vector for dengue and chikungunya transmission to humans?
    A. Anopheles
    B. Aedes
    C. Culex
    D. Mansonia
A

Aedes mosquitoes (especially Aedes aegypti and Aedes albopictus) are the principal vectors for dengue and chikungunya. Anopheles transmits malaria; Culex/Mansonia transmit other arboviruses and filarial species in some settings. CDC+1

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2
Q
  1. Which vector characteristic most explains why Anopheles mosquitoes are efficient malaria vectors?
    A. Daytime indoor biting only
    B. Preference for human blood and nighttime biting
    C. Small body size preventing blood feeding
    D. Transmits bacteria rather than protozoa
A

Anopheles species commonly bite at night and many prefer humans, facilitating transmission of Plasmodium parasites during sleeping hours — a key reason they efficiently spread malaria. CDC

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3
Q
  1. Which physiologic feature of Plasmodium falciparum infection explains the early predilection for fevers that cycle every 48–72 hours?
    A. Periodic synchronized rupture of infected erythrocytes releasing merozoites and pyrogenic substances
    B. Continuous low-level toxin release without cycles
    C. Direct airway inflammation causing fever
    D. Fungal co-infection causing cyclical fevers
A

The synchronous asexual erythrocytic cycle (merozoite release and RBC rupture) leads to periodic release of pyrogenic material and cyclical fevers (typically 48–72-hour periodicity depending on species). CDC

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4
Q
  1. Which component of the dengue virus life cycle directly causes the febrile and capillary-leak phases in severe disease?
    A. Viral replication in hepatocytes only
    B. Host immune response (cytokine-mediated) and endothelial dysfunction
    C. Direct bacterial co-infection
    D. Parasite invasion of RBCs
A

Severe dengue pathophysiology is driven mainly by host immune activation and cytokine-mediated endothelial dysfunction, which increases vascular permeability and can cause plasma leakage and shock. CDC+1

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5
Q
  1. In lymphatic filariasis, adult worms (e.g., Wuchereria bancrofti) primarily reside in which human structure?
    A. Pulmonary alveoli
    B. Lymphatic channels and lymph nodes
    C. Intestinal lumen
    D. Brain ventricles
A

Adult filarial worms inhabit lymphatic vessels and nodes, causing lymphatic dysfunction, lymphedema, and potential elephantiasis over time. World Health Organization+1

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6
Q
  1. Which blood stage of malaria is capable of infecting new mosquitoes when taken up in a blood meal?
    A. Asexual trophozoites
    B. Gametocytes
    C. Schizonts in spleen only
    D. Hypnozoites in the liver
A

Only sexual stages (male and female gametocytes) are infectious to mosquitoes; asexual erythrocytic forms are not taken up to continue the mosquito cycle. CDC

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7
Q
  1. Which physiologic mechanism best explains joint pain in chikungunya infection?
    A. Direct arthrotropic viral infection and immune-mediated inflammation of synovial tissues
    B. Hemorrhagic shock causing muscle cramps
    C. Parasite-induced RBC sickling in joints
    D. Bacterial septic arthritis only
A

Chikungunya virus has arthritogenic tropism and provokes immune-mediated inflammation in joint tissues, explaining severe acute and sometimes chronic arthralgia. World Health Organization+1

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8
Q
  1. Which anatomic/behavioral trait of Aedes aegypti increases household transmission risk?
    A. Preference for breeding in fast-flowing rivers
    B. Daytime biting and close association with human dwellings
    C. Only bites livestock at night
    D. Bites only in forest canopy
A

Aedes aegypti commonly breeds in peridomestic water containers and bites during the day, increasing close human contact and household transmission of dengue/chikungunya. CDC+1

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9
Q
  1. Which part of the mosquito is responsible for inoculating pathogens into the human host during feeding?
    A. Abdomen
    B. Proboscis (mouthparts)
    C. Hind legs
    D. Wings
A

The mosquito proboscis pierces skin and injects saliva containing pathogens; abdomen stores blood. CDC

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10
Q
  1. Which lifecycle stage of filarial worms circulates in peripheral blood and is picked up by mosquitoes?
    A. Microfilariae (larval stages)
    B. Adult worms in lymphatics
    C. Cysts in muscle tissue
    D. Hypnozoites in liver
A

Microfilariae circulate in blood (often nocturnally or diurnally depending on species) and are taken up by vectors; adults remain in lymphatics. World Health Organization+1

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11
Q
  1. Which physiologic change during severe dengue explains hemoconcentration seen on labs?
    A. Plasma leakage into interstitial/third spaces reduces intravascular plasma volume, increasing hematocrit
    B. Massive hemolysis increasing RBCs
    C. Decreased RBC production overnight
    D. Kidney failure concentrating blood cells
A

Plasma leakage due to increased vascular permeability concentrates red cells in the intravascular compartment, causing an elevated hematocrit — an important marker of severity. CDC

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12
Q
  1. Which host organ is the key site of dormant hypnozoites for Plasmodium vivax and ovale?
    A. Lung alveoli
    B. Hepatocytes (liver)
    C. Red blood cells
    D. Spleen
A

P. vivax and P. ovale form dormant hypnozoites in hepatocytes, which can relapse weeks to months later. CDC

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13
Q
  1. Which physiologic response contributes to splenic enlargement in malaria?
    A. Accumulation and removal of parasitized RBCs and immune-cell proliferation
    B. Fat deposition only
    C. Increased surfactant production
    D. Lymphatic obstruction like filariasis
A

The spleen enlarges due to phagocytosis of infected RBCs and immune hyperplasia, common in malaria. CDC

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14
Q
  1. Which mosquito-borne pathogen is most associated with hemorrhagic manifestations and shock in a subset of patients?
    A. Plasmodium falciparum
    B. Dengue virus
    C. Chikungunya virus
    D. Filarial nematodes
A

Dengue virus can cause severe dengue with plasma leakage, bleeding, and shock; malaria causes severe disease differently (e.g., cerebral malaria) but classic hemorrhagic syndrome is dengue. CDC

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15
Q
  1. Which physiologic feature of chikungunya distinguishes it from dengue in many cases?
    A. Prominent, often debilitating arthralgia that may persist for months
    B. High risk of vascular plasma leakage and shock
    C. Parasitic invasion of RBCs
    D. Chronic lymphatic obstruction
A

Chikungunya typically causes severe joint pain that can be prolonged; dengue more commonly causes plasma leakage and hemorrhagic complications. World Health Organization

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16
Q
  1. Which anatomic change in lymphatic filariasis leads to chronic elephantiasis?
    A. Repeated inflammation, obstruction, and fibrosis of lymphatics causing lymphedema and tissue hypertrophy
    B. Acute hemorrhage into limb tissues
    C. Direct muscle invasion causing atrophy
    D. Lung fibrosis
A

Chronic lymphatic damage with obstruction and fibrosis results in progressive lymphedema and elephantiasis. World Health Organization

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17
Q
  1. Which physiologic mechanism explains why insecticide-treated bed nets reduce malaria incidence?
    A. Nets physically block nocturnal biting Anopheles mosquitoes and insecticide deters or kills vectors
    B. Nets increase human body temperature deterring mosquitoes
    C. Nets reduce human breathing rate
    D. Nets sterilize skin
A

Bed nets physically reduce mosquito bites and treated nets also kill/deter Anopheles, lowering malaria transmission. CDC

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18
Q
  1. What is the key physiologic effect of microvascular sequestration in severe P. falciparum malaria?
    A. Obstruction of capillary blood flow by parasitized RBCs causing tissue hypoxia and organ dysfunction
    B. Immediate hemothorax
    C. Increased skin elasticity
    D. Rapid bone growth
A

P. falciparum–infected RBCs adhere to endothelium (sequestration), obstructing microcirculation and provoking ischemia (e.g., cerebral malaria). CDC

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19
Q
  1. Which physiologic factor determines whether filarial microfilariae are detectable in peripheral blood at night or during the day?
    A. Species-specific periodicity (nocturnal/diurnal) matching vector feeding habits
    B. Random fluctuations only
    C. Host age alone
    D. Mosquito size
A

Microfilariae show species-dependent periodicity timed to vector feeding (nocturnal vs diurnal), increasing transmission efficiency. NCBI

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20
Q
  1. Why does dengue infection sometimes cause thrombocytopenia?
    A. Bone marrow suppression, increased peripheral destruction, and consumption during plasma leakage/inflammation
    B. Increased RBC production uses platelets
    C. Platelets increase only in dengue
    D. Parasite invasion of platelets
A

Dengue-related bone marrow suppression plus immune-mediated destruction and consumption leads to thrombocytopenia, increasing bleeding risk. CDC

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21
Q
  1. Which physiologic site does Plasmodium first infect after an infected mosquito injects sporozoites?
    A. Hepatocytes (liver stage)
    B. Alveolar macrophages
    C. Peripheral nerves
    D. Lymph nodes only
A

Sporozoites rapidly reach the liver and infect hepatocytes, undergoing an exoerythrocytic (hepatic) stage before blood invasion. CDC

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22
Q
  1. Which host physiologic response contributes to persistent post-chikungunya arthralgia?
    A. Chronic immune-mediated inflammation and joint tissue immune activation
    B. Direct bone invasion by bacteria
    C. Parasite cyst formation in joints
    D. Permanent cartilage growth
A

Persistent joint pain after chikungunya is linked to ongoing immune-mediated inflammation in joint tissues for weeks to months. World Health Organization

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23
Q
  1. What physiologic change explains why pregnant women are at higher risk of severe malaria?
    A. Pregnancy-associated changes in immunity and placental sequestration of infected RBCs increasing parasite load
    B. Pregnancy prevents mosquito bites
    C. Placenta filters parasites out completely
    D. Pregnancy increases bone marrow function only
A

Pregnancy alters immune responses and the placenta can sequester infected RBCs, increasing risk of severe disease and poor outcomes. CDC

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24
Q
  1. Which physiologic effect of severe malaria primarily leads to metabolic acidosis?
    A. Tissue hypoxia from microvascular obstruction and high metabolic demand producing lactic acidosis
    B. Excess ventilation eliminating CO₂
    C. Alkalosis from hyperventilation
    D. Decreased production of lactic acid
A

Microvascular obstruction → tissue hypoxia → anaerobic metabolism and lactic acidosis manifesting as metabolic acidosis in severe malaria. CDC

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25
25. Which physiologic condition allows dengue, chikungunya, and Zika to co-circulate and complicate diagnosis in certain regions? A. Shared Aedes mosquito vectors and overlapping ecology/seasonality leading to similar clinical presentations B. Completely different vectors eliminating overlap C. Seasonal separation always prevents co-infection D. Vector immunity in humans
Shared vectors (Aedes spp.) and overlapping ecology allow co-circulation and similar early symptoms, complicating clinical differentiation. CDC+1
26
1. What pathophysiologic process most explains plasma leakage in severe dengue? A. Immune-mediated endothelial dysfunction and cytokine surge B. Direct viral destruction of RBCs C. Parasite sequestration in capillaries D. Excess platelet production
Severe dengue involves cytokine-induced endothelial permeability, not RBC lysis. Plasma leakage distinguishes severe dengue from other arboviral illnesses.
27
2. In malaria, why does Plasmodium falciparum cause more severe disease than other species? A. Ability of infected RBCs to adhere to microvascular endothelium (sequestration) B. Very slow replication C. Lack of liver involvement D. Rapid immune clearance
P. falciparum causes sequestration, obstructing microcirculation and leading to cerebral malaria and organ failure.
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3. Why do dengue patients experience thrombocytopenia? A. Bone marrow suppression and peripheral platelet destruction B. Parasite invasion of platelets C. Increased platelet production D. Hypercoagulation only
Dengue reduces platelet count via bone marrow suppression and immune-mediated destruction, increasing bleeding risk.
29
4. What pathophysiologic mechanism leads to severe joint pain in chikungunya? A. Viral replication in joint tissues and chronic immune activation B. Bone marrow hyperplasia C. Complete destruction of cartilage D. RBC invasion of synovial fluid
Chikungunya is arthritogenic, causing persistent inflammatory responses in joints.
30
5. Why do Wuchereria bancrofti infections eventually cause elephantiasis? A. Chronic lymphatic inflammation → fibrosis → permanent obstruction B. Acute toxin release into lymphatics C. Destruction of bone marrow D. Direct vascular occlusion by eggs
Long-term lymphatic injury produces fibrosis and obstruction, resulting in chronic lymphedema.
31
6. What causes cyclic fevers in malaria? A. Synchronized rupture of RBCs releasing pyrogens B. Viral antigen cycling C. Bone marrow hypoxia D. Hepatocyte rupture only
Malaria fevers correspond to RBC rupture, releasing pyrogenic substances in synchronized cycles.
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7. How does secondary dengue infection increase risk of severe dengue? A. Antibody-dependent enhancement enhances viral entry and immune activation B. Stronger neutralizing antibodies prevent infection C. Parasite replication increases D. Mosquito bites become more frequent
Preexisting antibodies can enhance viral uptake, increasing severity due to heightened immune responses.
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8. Why does malaria commonly cause anemia? A. Hemolysis of infected and uninfected RBCs B. Bone marrow overproduction C. Increased RBC lifespan D. Blocked iron absorption only
Malaria destroys RBCs via direct hemolysis and immune clearance of uninfected cells.
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9. Why can severe malaria cause metabolic acidosis? A. Tissue hypoxia from microvascular obstruction → lactic acidosis B. Excess bicarbonate production C. Decreased respiratory rate D. Liver detoxification
Microvascular obstruction → tissue hypoxia, leading to anaerobic metabolism and lactic acidosis.
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10. What explains the risk of shock in severe dengue? A. Sudden plasma leakage reducing intravascular volume B. Massive hemolysis only C. Hyperkalemia D. Excess sodium retention
Severe dengue shock results from plasma leakage and capillary permeability, not hemolysis.
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11. In lymphatic filariasis, why are microfilariae more detectable at night? A. Nocturnal periodicity synchronized with mosquito feeding patterns B. Random distribution throughout day C. Host sleep reduces immune activity D. Microfilariae die in daylight
Many species show nocturnal periodicity, coordinating with vector feeding and enhancing transmission.
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12. Why does Plasmodium vivax relapse after apparent cure? A. Hypnozoites persist in liver and reactivate later B. RBC invasion restarts regularly C. Immune suppression cycles D. Mosquitoes reinfect instantly
P. vivax forms dormant liver stages (hypnozoites) that can reactivate months later.
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13. Why is cerebral malaria more common in P. falciparum infection? A. Sequestration of infected RBCs in brain microvasculature B. Viral co-infection C. Filariasis interaction D. Lack of immune response
Falciparum-infected RBCs adhere to endothelial cells, blocking cerebral capillaries.
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14. Why do chikungunya symptoms sometimes last months? A. Persistent immune activation in joints and viral RNA remnants B. Parasite dormancy C. Viral integration into DNA D. Bone destruction
Post-viral inflammatory reactions produce chronic arthralgia.
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15. Why does dengue sometimes cause liver involvement? A. Viral replication in hepatocytes and immune-mediated injury B. Direct RBC invasion C. Lymphatic obstruction D. Parasite cysts in liver
Dengue infects hepatocytes, causing transaminitis and sometimes liver failure.
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16. What causes pulmonary edema in severe malaria? A. Increased capillary permeability and inflammatory lung injury B. Parasite growth in alveoli C. Bronchoconstriction D. Lymphatic overload
Malaria can trigger ARDS-like capillary leak, causing pulmonary edema.
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17. Why does filariasis increase susceptibility to skin infections? A. Lymphatic obstruction impairs immune drainage and skin integrity B. Viral co-infection C. Bone infection D. Hyperpigmentation
Chronic lymphedema impairs immune function, increasing risk of secondary bacterial infections.
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18. Why does malaria impair splenic function over time? A. Overactivity from clearing infected RBCs leads to congestion and dysfunction B. Direct viral invasion C. Parasite cysts form D. Increased fat deposition
The spleen becomes overloaded, causing congestion and decreased filtering ability.
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19. Why can dengue lead to severe abdominal pain? A. Plasma leakage into peritoneal cavity and visceral edema B. RBC invasion of intestines C. Parasite cysts D. Liver shrinkage
Severe dengue often involves peritoneal/visceral edema from vascular leakage.
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20. What pathophysiologic mechanism causes lymphangitis in acute filariasis? A. Immune response to dying microfilariae in lymphatics B. Direct invasion of arteries C. Bone marrow infiltration D. Parasitic RBC invasion
Acute filarial attacks occur when microfilariae die, triggering intense lymphatic inflammation.
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21. Which mechanism causes hemoglobinuria (“blackwater fever”) in severe falciparum malaria? A. Massive intravascular hemolysis B. Liver failure C. Kidney obstruction by worms D. Platelet destruction
Severe malaria can cause massive hemolysis, leading to hemoglobinuria.
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22. Why are pregnant women at higher risk of severe dengue? A. Increased vascular permeability and immune modulation B. RBC destruction C. Parasite growth in placenta D. Lymphatic obstruction
Pregnancy increases vascular permeability and modifies immune function, heightening dengue severity.
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23. Why does malaria cause splenomegaly more in chronic exposure regions? A. Repeated infections cause hyperplasia and congestion of splenic tissue B. Bone enlargement C. Filariasis co-infection D. Chronic dehydration
Frequent infections cause splenic hyperplasia.
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24. What causes shock in miliary filariasis? A. Systemic inflammatory response and endotoxin-like reactions from dying parasites B. Liver rupture C. Massive hemorrhage D. Lung parasite cysts
Dying worms may trigger severe inflammatory responses, causing systemic instability.
50
25. Why can chikungunya mimic rheumatoid arthritis? A. Chronic inflammatory synovitis resembling autoimmune patterns B. RBC invasion C. Viral persistence in cartilage forming cysts D. Lymphatic obstruction
Chikungunya can cause chronic synovitis, presenting like RA.
51
1. A patient returns from a dengue-endemic area with high fever, severe myalgia, retro-orbital pain, and a faint maculopapular rash. Which combination best supports a working clinical diagnosis of acute dengue? A. High fever, severe myalgia, retro-orbital pain, rash B. Painless jaundice only C. Isolated chronic cough D. Painless localized swelling
The classic dengue presentation includes abrupt high fever, severe myalgia (“breakbone” pain), retro-orbital pain, and often a maculopapular rash. Jaundice, chronic cough, or painless localized swelling are not typical initial dengue features.
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2. A traveler presents with paroxysms of fever, chills, and sweats every 48 hours. Which diagnostic specimen and test most reliably confirm malaria? A. Thick and thin blood smears for microscopy B. Throat swab culture C. Urine dipstick only D. Chest x-ray
Diagnosis of malaria is confirmed by thick (for sensitivity) and thin (for speciation) blood smears examined microscopically; throat swabs/urine/x-ray are not diagnostic for malaria.
53
3. A patient with severe dengue is noted to have a rising hematocrit and falling blood pressure. Which bedside diagnostic sign is most consistent with plasma leakage? A. Hemoconcentration (rising hematocrit) and hypotension B. Increased urine output only C. Worsening hyperglycemia D. Sudden leukocytosis
Rising hematocrit with hypotension indicates intravascular plasma loss (hemoconcentration) due to vascular leakage—classic for severe dengue. Increased urine etc. do not explain plasma leakage.
54
4. A febrile patient has severe joint pains that began abruptly after a mosquito bite; synovitis is suspected. Which test(s) can help confirm chikungunya infection in the acute phase? A. Serum RT-PCR for viral RNA and acute-phase IgM serology B. Blood culture for bacteria only C. Fecal ova and parasite exam D. ANA (antinuclear antibody) only
In acute chikungunya, RT-PCR detects viral RNA early; IgM appears soon after—these confirm recent infection. Bacterial cultures, stool O&P, or ANA are not appropriate acute diagnostics.
55
5. A patient with suspected lymphatic filariasis shows chronic unilateral lower-limb swelling. Which diagnostic test is most useful to demonstrate active microfilaremia? A. Night-timed peripheral blood smear for microfilariae (or concentration techniques) B. Throat culture C. Random urine pregnancy test D. Skin prick for allergens
Microfilariae are often detectable in peripheral blood with species-dependent periodicity (nocturnal or diurnal), so timed blood smears or concentration methods are the key diagnostic test.
56
6. In a patient with suspected severe P. falciparum malaria, which laboratory finding is most concerning for poor prognosis? A. Elevated lactate and metabolic acidosis B. Slightly elevated HDL C. Normal hemoglobin only D. Isolated mild hypokalemia
Elevated lactate and metabolic acidosis indicate tissue hypoxia from microvascular obstruction and are markers of severe malaria and poor prognosis.
57
7. Which early laboratory test is most useful to identify dengue virus infection within the first 5 days of symptoms? A. NS1 antigen detection (rapid or ELISA) and/or RT-PCR B. Stool culture C. Blood film for parasites only D. Serum electrolytes only
NS1 antigen detection and RT-PCR are sensitive in early dengue (first 5 days). Stool cultures/parasite films/electrolytes do not diagnose acute dengue.
58
8. A patient has persistent high fever, confusion, and focal neurologic signs after returning from a malaria area. Which diagnostic step is essential immediately? A. Immediate thick and thin blood smears and urgent evaluation for cerebral malaria (including rapid parasitemia quantification) B. Delay labs for 48 hours C. Only test for dengue NS1 D. Obtain allergy testing
Neurologic signs suggest cerebral malaria, an emergency; prompt blood smears and parasitemia assessment are essential. Delaying tests or only doing dengue tests would risk fatal delay.
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9. A clinician suspects dengue hemorrhagic fever. Which combination of lab abnormalities supports this diagnosis? A. Thrombocytopenia, rising hematocrit, hemoconcentration, and evidence of plasma leakage B. Marked neutrophilic leukocytosis only C. Elevated creatine kinase only D. Hypercalcemia only
Dengue hemorrhagic manifestations are associated with thrombocytopenia and hemoconcentration from plasma leakage; neutrophilic leukocytosis is not characteristic.
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10. A patient presents with fever and severe anemia after travel; labs show hemoglobinuria and black-colored urine. Which malaria complication is most likely? A. Massive intravascular hemolysis (blackwater fever) often associated with falciparum infection B. Viral hepatitis only C. Isolated upper respiratory infection D. Dehydration without hemolysis
Blackwater fever is due to massive hemolysis with hemoglobinuria, historically linked to falciparum malaria and sometimes certain antimalarial exposures.