Infectious And Tropical Flashcards
(482 cards)
1
Q
What is malaria and what is the etiology?
A
Malaria is a life-threatening parasitic disease caused by protozoa of the genus Plasmodium. The species affecting humans include P. falciparum, P. vivax, P. ovale, and P. malariae. Plasmodium falciparum causes the most severe form of malaria and can lead to death if untreated.
2
Q
What are the primary vectors for malaria transmission?
A
Malaria is transmitted by Anopheles mosquitoes, which are most active between dusk and dawn. These mosquitoes pick up the parasite from infected human blood and transmit it during subsequent bites.
3
Q
What are the stages of the malaria life cycle?
A
The malaria life cycle includes the mosquito stage (sporogonic cycle) and the human liver and red blood cell stages (schizogony). In the liver, merozoites mature, and in red blood cells, they undergo schizogony, leading to the release of merozoites that infect other RBCs.
4
Q
How does Plasmodium falciparum cause severe disease?
A
Plasmodium falciparum causes severe malaria through sequestration of infected red blood cells in microvasculature, leading to cerebral malaria, organ failure, and increased parasite burden. It can also cause metabolic acidosis and hypoglycemia.
5
Q
What is cerebral malaria and how does it present?
A
Cerebral malaria occurs when infected RBCs block cerebral blood flow, causing neurological symptoms such as seizures, altered consciousness, coma, and potential death. This is a medical emergency that requires prompt treatment.
6
Q
What is the role of G6PD deficiency in malaria?
A
Glucose-6-phosphate dehydrogenase (G6PD) deficiency is common in malaria-endemic areas. It can increase the risk of hemolytic anemia after taking antimalarial drugs like primaquine, which should be avoided in individuals with G6PD deficiency.
7
Q
What is the clinical presentation of uncomplicated malaria?
A
Symptoms of uncomplicated malaria include high fever, chills, sweating, headache, nausea, vomiting, myalgia, and general malaise. These symptoms typically occur in periodic cycles (every 48–72 hours) corresponding to the release of merozoites from red blood cells.
8
Q
What are the classic signs of severe malaria?
A
Severe malaria includes symptoms such as altered consciousness (due to cerebral malaria), severe anemia, metabolic acidosis, renal failure, hypoglycemia, respiratory distress, and shock.
9
Q
What are the diagnostic tools for malaria?
A
Malaria diagnosis is confirmed by microscopic examination of blood smears (thick and thin films), rapid diagnostic tests (RDTs) that detect Plasmodium antigens, and PCR tests to confirm the species and assess parasitemia.
10
Q
How is a thick blood smear different from a thin blood smear in malaria diagnosis?
A
A thick blood smear is used for detecting high parasitemia and is more sensitive, while the thin smear helps identify the species of Plasmodium based on the morphology of infected red blood cells.
11
Q
What is the management of uncomplicated malaria caused by Plasmodium falciparum?
A
First-line treatment for uncomplicated malaria caused by P. falciparum includes artemisinin-based combination therapy (ACT), such as artemether-lumefantrine or artesunate-amodiaquine. These medications rapidly reduce parasite load.
12
Q
What is the management of severe malaria caused by Plasmodium falciparum?
A
Severe malaria requires intravenous artesunate (first-line) or intravenous quinine, followed by ACT when the patient stabilizes. Patients should also be monitored for complications like hypoglycemia, acidosis, and anemia.
13
Q
What are the complications of untreated malaria?
A
Untreated malaria can lead to cerebral malaria, organ failure (liver, kidneys, lungs), severe anemia, and death. P. vivax and P. ovale can also cause relapse by reactivating liver hypnozoites.
14
Q
What are the features of hypnozoite relapse in P. vivax and P. ovale?
A
P. vivax and P. ovale can form dormant liver stages (hypnozoites), which can reactivate months or even years after the initial infection, causing relapsing malaria. This requires treatment with primaquine to eliminate the hypnozoites.
15
Q
How is malaria prevented in endemic areas?
A
Prevention strategies include insecticide-treated bed nets (ITNs), indoor residual spraying (IRS), environmental control of mosquito breeding sites, and chemoprophylaxis for travelers to endemic areas. The use of antimalarial drugs, like doxycycline, is also recommended for travelers.
16
Q
What are the challenges in malaria control?
A
Challenges include insecticide resistance in mosquitoes, drug resistance in Plasmodium, and the high cost of malaria control programs. There is also the challenge of compliance with malaria chemoprophylaxis in travelers.
17
Q
How is malaria treated during pregnancy?
A
Pregnant women are at higher risk of severe malaria. Artemisinin-based therapies are recommended in the second and third trimesters, and quinine plus clindamycin is used in the first trimester. Malaria during pregnancy can cause miscarriage, preterm delivery, and low birth weight.
18
Q
What is the role of malaria vaccines?
A
The RTS,S/AS01 (Mosquirix) malaria vaccine has been shown to reduce malaria incidence in children in sub-Saharan Africa. It targets the sporozoite stage of Plasmodium falciparum and is used in conjunction with other preventive measures.
19
Q
What are the indications for hospitalization in malaria?
A
Hospitalization is required for severe malaria, cerebral malaria, significant anemia (hemoglobin <5 g/dL), renal failure, hypoglycemia, or respiratory distress. Patients should be monitored for complications and treated with intravenous medications.
20
Q
What are the key differences between malaria and other febrile illnesses in tropical regions?
A
Malaria must be differentiated from dengue, typhoid fever, leptospirosis, and rickettsial infections based on clinical features, epidemiology, and laboratory tests (e.g., blood smears, RDTs, or PCR). A careful travel history and the use of diagnostic tests are essential.
21
Q
What is the importance of parasitemia quantification in malaria treatment?
A
Quantifying parasitemia helps guide the treatment decision. A parasitemia level >5% is considered high and is associated with severe disease, requiring aggressive treatment and monitoring.
22
Q
What is the epidemiology of malaria worldwide?
A
Malaria is endemic in sub-Saharan Africa, Southeast Asia, the Indian subcontinent, and parts of Central and South America. In Africa, children under 5 years old and pregnant women are most vulnerable to severe malaria and death.
23
Q
What is dengue fever and its causative agent?
A
Dengue fever is a mosquito-borne viral infection caused by the dengue virus (DENV), a flavivirus with four distinct serotypes: DENV-1, DENV-2, DENV-3, and DENV-4.
24
Q
How is dengue virus transmitted?
A
Dengue is transmitted by the bite of Aedes mosquitoes, primarily Aedes aegypti and Aedes albopictus, which are day-biting and breed in stagnant water.
25
What are the phases of dengue infection?
The illness progresses through three phases: febrile phase, critical phase (with plasma leakage), and recovery phase.
26
What are the clinical features of the febrile phase?
Sudden onset of high-grade fever, headache (retro-orbital), myalgia, arthralgia, skin flushing, anorexia, nausea, and sometimes a maculopapular rash.
27
What is the hallmark of the critical phase in dengue?
Plasma leakage leading to hemoconcentration, pleural effusion, ascites, hypovolemia, and potentially dengue shock syndrome (DSS).
28
What are the warning signs of severe dengue?
Persistent vomiting, abdominal pain, mucosal bleeding, lethargy, hepatomegaly, increasing hematocrit with rapid drop in platelets, and clinical fluid accumulation.
29
What laboratory findings support a diagnosis of dengue?
Leukopenia, thrombocytopenia, elevated hematocrit, elevated liver enzymes (AST>ALT), and positive NS1 antigen or IgM/IgG serology.
30
How is dengue fever diagnosed?
Diagnosis is made by clinical criteria and confirmed by detection of NS1 antigen (early), IgM/IgG antibodies (later), or RT-PCR.
31
What is the pathophysiology of dengue shock syndrome?
DSS results from increased capillary permeability leading to plasma leakage, hypovolemia, and shock with a narrow pulse pressure (<20 mmHg).
32
How is mild dengue managed?
Outpatient supportive care including oral rehydration, paracetamol for fever, avoidance of NSAIDs, and close monitoring for warning signs.
33
When should hospitalization be considered in dengue?
Hospitalization is needed for patients with warning signs, dehydration, bleeding, persistent vomiting, or lab abnormalities like high hematocrit and low platelets.
34
What is the fluid management strategy during the critical phase?
Controlled IV fluids guided by clinical assessment and hematocrit, aiming to avoid both hypovolemia and fluid overload.
35
What are the signs of fluid overload during dengue management?
Breathing: Rapid breathing, crackles, distress
Swelling: Facial puffiness, ascites, pleural effusions
Vitals: Widened pulse pressure, bradycardia, hypertension
Hematocrit: Sudden drop without bleeding
Urine: Decreased output
Imaging: Pulmonary edema on X-ray/ultrasound
Action: Stop IV fluids, give oxygen, consider diuretics if stable.
36
What are the complications of severe dengue?
Dengue shock syndrome, bleeding (GI or intracranial), liver failure, myocarditis, encephalitis, and multi-organ failure.
37
How is dengue managed during the recovery phase?
Gradual tapering of fluids as capillary leakage resolves, with attention to signs of hypervolemia and diuresis.
38
How does secondary dengue infection differ from primary infection?
Secondary infection with a different DENV serotype increases the risk of antibody-dependent enhancement, leading to severe disease.
39
What are the hematological changes seen in dengue?
Progressive thrombocytopenia, leukopenia, elevated hematocrit due to hemoconcentration, and prolonged PT/INR in severe cases.
40
What are the WHO classifications of dengue?
2011 WHO guidelines classify dengue as dengue without warning signs, dengue with warning signs, and severe dengue.
41
What is the role of platelet transfusion in dengue?
Platelet transfusion is not indicated solely based on low counts; it is reserved for active bleeding or invasive procedures.
42
How can dengue be prevented?
Vector control (eliminating mosquito breeding sites), personal protection (repellents, bed nets), and dengue vaccine (limited use in seropositive individuals).
43
What is typhoid fever and its causative organism?
Typhoid fever is a systemic bacterial infection caused by Salmonella enterica serotype Typhi. Paratyphoid fever is caused by Salmonella Paratyphi A, B, or C.
44
How is typhoid fever transmitted?
It is transmitted through the fecal-oral route, commonly via contaminated food or water, particularly in areas with poor sanitation.
45
What is the pathogenesis of typhoid fever?
S. Typhi enters the intestinal mucosa, invades macrophages, and spreads through the lymphatic and reticuloendothelial systems, leading to bacteremia and systemic symptoms.
46
What are the early symptoms of typhoid fever in children?
Prolonged fever, malaise, anorexia, abdominal pain, headache, and constipation are common early symptoms.
47
What are the late symptoms of typhoid fever?
Splenomegaly, hepatomegaly, rose spots on the abdomen, diarrhea (especially in older children), and altered mental status in severe cases.
48
What is the characteristic fever pattern in typhoid?
Step-ladder pattern—fever gradually increases in a stepwise fashion over several days, often reaching >39°C.
49
How is typhoid diagnosed?
Blood culture is the gold standard, especially during the first week. Stool and urine cultures may become positive later. Widal test has limited utility.
50
What are the limitations of the Widal test?
Cross-reactivity, poor sensitivity and specificity, and need for baseline titers in endemic areas make it unreliable for diagnosis.
51
What are the complications of untreated typhoid fever?
Intestinal perforation, GI bleeding, encephalopathy, hepatitis, myocarditis, and hemophagocytic syndrome.
52
When does intestinal perforation typically occur in typhoid?
Usually in the third week of illness, presenting with sudden abdominal pain, peritonitis, and sepsis.
53
How is uncomplicated typhoid fever treated?
First-line antibiotics include azithromycin, cefixime, or ceftriaxone. Fluoroquinolones are avoided due to rising resistance.
54
How is severe typhoid fever treated?
IV ceftriaxone is preferred. Consider azithromycin or meropenem for multi-drug resistant (MDR) or extensively drug-resistant (XDR) strains.
55
What is the duration of antibiotic therapy in typhoid?
Usually 7–14 days depending on the severity and response to treatment. Shorter courses may be used for azithromycin.
56
What is chronic carrier state in typhoid?
Defined as excretion of S. Typhi in stool or urine for more than 12 months. Carriers are a reservoir for transmission.
57
How is chronic typhoid carriage treated?
Prolonged antibiotic therapy with amoxicillin or ciprofloxacin, and cholecystectomy in select cases if gallbladder involvement is suspected.
58
What vaccines are available for typhoid prevention?
Ty21a oral live attenuated vaccine and Vi polysaccharide injectable vaccine are available. Newer conjugate vaccines (TCV) offer better immunogenicity and longer protection.
59
When is typhoid vaccination recommended?
In endemic areas, for travelers, and during outbreaks. TCV is given from 6 months of age in high-risk areas.
60
How is typhoid fever prevented?
Improved sanitation, access to clean water, hand hygiene, food safety practices, and vaccination.
61
What is the role of stool culture in typhoid diagnosis?
Stool culture is useful during the second and third weeks, especially in suspected chronic carriers or relapsed cases.
62
What are the indicators of poor prognosis in typhoid fever?
High fever >7 days, altered sensorium, leukopenia, thrombocytopenia, elevated liver enzymes, intestinal bleeding, and perforation.
63
What causes tuberculosis (TB) in children?
TB is caused by Mycobacterium tuberculosis, an acid-fast bacillus transmitted via airborne droplets from infected individuals.
64
What are the common sites of TB infection in children?
Pulmonary TB is most common, but extrapulmonary TB can affect lymph nodes, meninges, bones, joints, gastrointestinal tract, and miliary dissemination.
65
What are the typical symptoms of pulmonary TB in children?
Chronic cough (>2 weeks), weight loss or failure to thrive, fever, night sweats, and fatigue.
66
How is TB transmitted?
Via inhalation of airborne droplets expelled by a person with active pulmonary TB. Children usually acquire TB from adult household contacts.
67
What are the stages of TB infection?
Primary infection, latent TB infection (LTBI), and reactivation disease. Children are more prone to progression from primary infection to active disease.
68
What is the Mantoux tuberculin skin test (TST)?
A test where 0.1 mL of purified protein derivative (PPD) is injected intradermally. Induration is measured at 48–72 hours. ≥10 mm is positive in high-risk children.
69
What are the limitations of the TST?
False positives from BCG vaccination or non-TB mycobacteria; false negatives in malnutrition, HIV, or early infection.
70
What is the role of interferon-gamma release assays (IGRAs)?
IGRAs (e.g., QuantiFERON-TB Gold) measure immune response to TB-specific antigens and are useful for diagnosing LTBI, especially in BCG-vaccinated children.
71
How is pulmonary TB diagnosed?
**1. Clinical Presentation:**
- Chronic cough (>2-3 weeks), weight loss, fever, night sweats, fatigue
- High-risk children: recent TB contact, immunocompromised, malnourished
**2. Tuberculin Skin Test (TST / Mantoux Test):**
- Positive if:
- ≥5 mm (high-risk, immunocompromised, close contact)
- ≥10 mm (moderate-risk)
- ≥15 mm (low-risk)
**3. Interferon-Gamma Release Assays (IGRAs):**
- Not affected by BCG vaccination
- Examples: QuantiFERON-TB Gold, T-SPOT.TB
**4. Chest Radiography:**
- Hilar/mediastinal lymphadenopathy, Ghon complex, lobar consolidation, pleural effusion, miliary pattern
**5. Microbiological Testing:**
- Sputum microscopy, culture, GeneXpert MTB/RIF
- Alternative samples: gastric aspirates, BAL, nasopharyngeal aspirates
**6. Rapid Molecular Tests:**
- GeneXpert MTB/RIF: rapid detection and rifampicin resistance
- Line Probe Assays (LPA): drug resistance detection
**7. Other Tests:**
- Histopathology (caseating granulomas)
- Lumbar puncture for TB meningitis
- MRI/CT for miliary or spine involvement
**8. Contact Tracing:**
- Screening household contacts for active or latent TB
**9. HIV Testing:**
- Mandatory due to high TB-HIV co-infection rates
72
What are the radiological findings in pediatric pulmonary TB?
Hilar lymphadenopathy, segmental consolidation, miliary pattern, or cavitary lesions in older children.
73
What is the treatment regimen for drug-sensitive TB?
2 months of intensive phase with isoniazid (H), rifampin (R), pyrazinamide (Z), and ethambutol (E) followed by 4 months of continuation phase with H and R.
74
What are the doses of first-line TB drugs in children?
Isoniazid: 10 mg/kg/day, Rifampin: 15 mg/kg/day, Pyrazinamide: 35 mg/kg/day, Ethambutol: 20 mg/kg/day.
75
How is TB meningitis managed in children?
Initiate HRZE regimen plus corticosteroids (e.g., dexamethasone) for 8–12 weeks. Treatment duration is usually extended to 9–12 months.
76
What are the side effects of TB medications?
1. Isoniazid (INH)
Hepatotoxicity
Peripheral neuropathy
Pyridoxine (vitamin B6) is given to prevent neuropathy
2. Rifampicin (Rifampin)
Orange discoloration of body fluids
Gastrointestinal upset
Drug interactions due to CYP450 enzyme induction
3. Pyrazinamide (PZA)
Joint pain (arthralgia)
Elevated uric acid (hyperuricemia)
Gastrointestinal upset
4. Ethambutol (EMB)
Visual problems (optic neuritis: blurred vision, red-green color blindness)
Requires regular vision tests
5. Streptomycin
Hearing loss and balance issues (ototoxicity)
Kidney toxicity (nephrotoxicity)
Important Notes:
Monitor liver function due to risk of hepatotoxicity (especially with INH, Rifampin, and PZA)
Adjust or stop treatment if significant side effects appear.
77
How is latent TB infection treated in children?
Options include 6–9 months of isoniazid monotherapy, or 3 months of isoniazid + rifampin, depending on adherence and drug tolerance.
78
What is multidrug-resistant TB (MDR-TB)?
TB resistant to at least isoniazid and rifampin. Requires second-line drugs like fluoroquinolones, injectable agents, and longer treatment duration.
79
What are the signs of TB in infants and young children?
Failure to thrive, persistent pneumonia not responding to antibiotics, hepatosplenomegaly, and lymphadenopathy.
80
What are the common extrapulmonary forms of TB in children?
Lymph node TB, TB meningitis, abdominal TB, bone/joint TB, and miliary TB.
81
What is the role of the BCG vaccine?
BCG (Bacillus Calmette–Guérin) is administered at birth in endemic countries to protect against severe forms of TB like miliary TB and TB meningitis.
82
When should a child be screened for TB?
Children with household TB contacts, HIV-positive children, those with malnutrition, or presenting with persistent cough/fever should be screened.
83
What is leptospirosis and its causative organism?
Leptospirosis is a zoonotic bacterial infection caused by pathogenic spirochetes of the genus Leptospira, particularly Leptospira interrogans.
84
How is leptospirosis transmitted?
Humans acquire the infection through contact with water, soil, or food contaminated with urine of infected animals, especially rodents. Entry occurs via mucous membranes or abraded skin.
85
What are common environmental risk factors for leptospirosis?
Exposure to floodwater, poor sanitation, recreational water activities, and living in areas with rodent infestation.
86
What are the clinical phases of leptospirosis?
It typically presents in two phases: a septicemic (acute) phase and an immune (delayed) phase, separated by a brief asymptomatic period.
87
What are the symptoms of the acute/septicemic phase?
Sudden onset of high fever, headache, myalgia (especially calf tenderness), conjunctival suffusion, nausea, vomiting, and abdominal pain.
88
What are the features of the immune phase?
Meningeal signs, uveitis, rash, hematuria, proteinuria, and complications such as hepatitis, renal failure, and myocarditis.
89
What is Weil's disease?
A severe form of leptospirosis characterized by jaundice, acute kidney injury, hemorrhagic manifestations, and sometimes pulmonary involvement.
90
What are pulmonary manifestations of leptospirosis?
Cough, dyspnea, hemoptysis, and pulmonary hemorrhage, which may progress to acute respiratory distress syndrome (ARDS).
91
What are the key laboratory findings in leptospirosis?
Leukocytosis with left shift, thrombocytopenia, elevated creatinine, elevated liver enzymes, proteinuria, and electrolyte abnormalities (e.g., hypokalemia).
92
How is leptospirosis diagnosed?
Diagnosis is confirmed by serology (MAT or ELISA for Leptospira IgM), PCR for Leptospira DNA, or culture (rarely used).
93
What is the role of the microscopic agglutination test (MAT)?
MAT is the gold standard serologic test for leptospirosis, detecting antibodies against multiple Leptospira serovars.
94
What imaging findings support a diagnosis of leptospirosis?
Chest X-ray may show bilateral pulmonary infiltrates or hemorrhage in severe cases. Renal ultrasound may show enlarged echogenic kidneys.
95
What is the treatment for mild leptospirosis?
Oral doxycycline or amoxicillin for 5–7 days. Azithromycin is an alternative for younger children.
96
What is the treatment for severe leptospirosis?
Intravenous penicillin G or third-generation cephalosporins (e.g., ceftriaxone) for 7–10 days.
97
When should leptospirosis be suspected in children?
Consider in febrile children with exposure to contaminated water, conjunctival suffusion, myalgia, renal/liver dysfunction, or aseptic meningitis.
98
What is the prognosis of leptospirosis?
Most children recover with appropriate therapy. However, severe forms like Weil’s disease have higher mortality, especially with pulmonary hemorrhage.
99
What are the differential diagnoses for leptospirosis?
Dengue fever, typhoid, viral hepatitis, malaria, rickettsial infections, and HUS.
100
How is leptospirosis prevented?
Avoidance of contaminated water, rodent control, protective clothing, and doxycycline prophylaxis in high-risk areas.
101
What is the role of doxycycline prophylaxis?
Doxycycline 200 mg weekly can be used as chemoprophylaxis for travelers or individuals exposed to high-risk environments during outbreaks.
102
What are the indications for hospitalization in leptospirosis?
Severe symptoms such as jaundice, hypotension, renal failure, altered consciousness, hemorrhage, or respiratory distress.
103
What is kala-azar and what causes it?
Kala-azar, or visceral leishmaniasis (VL), is caused by protozoan parasites of the Leishmania donovani complex, transmitted by the bite of infected female sandflies (Phlebotomus species).
104
What is the typical geographic distribution of kala-azar?
Kala-azar is endemic in parts of South Asia (India, Bangladesh, Nepal), East Africa (Sudan, Ethiopia), and South America.
105
What is the incubation period of kala-azar?
The incubation period ranges from 2 weeks to several months after the bite of an infected sandfly.
106
What is the classic clinical presentation of kala-azar in children?
Prolonged fever, weight loss, hepatosplenomegaly (especially splenomegaly), pallor, pancytopenia, and hypergammaglobulinemia.
107
What are the signs of severe or advanced visceral leishmaniasis?
Massive splenomegaly, severe anemia, thrombocytopenia, secondary bacterial infections, edema, and wasting.
108
How is kala-azar diagnosed?
Diagnosis is confirmed by identification of amastigotes (LD bodies) in splenic aspirate (most sensitive), bone marrow, or lymph nodes, or by rK39 antigen test (serology).
109
What is the role of the rK39 test?
The rK39 rapid diagnostic test detects antibodies against Leishmania; it is highly sensitive in endemic areas and widely used for initial screening.
110
Why is splenic aspiration the most sensitive diagnostic method?
Splenic aspirate has the highest parasite load, but carries a risk of bleeding; it is reserved for experienced centers.
111
What hematologic abnormalities are common in kala-azar?
Pancytopenia (anemia, leukopenia, thrombocytopenia), hypergammaglobulinemia, and hypoalbuminemia.
112
What is the first-line treatment for kala-azar in children?
In Sudan, the first-line treatment for visceral leishmaniasis (kala-azar) in children is a combination of sodium stibogluconate (SSG) and paromomycin (PM). This regimen involves daily intramuscular injections of SSG at 20 mg/kg and PM at 15 mg/kg for 17 days.
113
What are alternative treatments for kala-azar?
A. Liposomal Amphotericin B (AmBisome)
Effective in: India, HIV patients, pregnancy
Advantages: Very effective, fewer side effects
Limitations: Expensive, cold-chain, lower efficacy in East Africa
B. Oral Miltefosine
Use: Monotherapy or part of combination therapy
Advantages: Oral, outpatient-friendly
Limitations: Teratogenic, GI side effects, not used in pregnancy
C. Miltefosine + Paromomycin
Emerging regimen in East Africa
Advantages: Shorter course (14–17 days), fewer injections, >90% efficacy
Current Status: Under review, promising for replacing SSG/PM
D. Amphotericin B Deoxycholate
Use: Older IV drug used when liposomal form is unavailable
Limitations: Nephrotoxicity, prolonged course, infusion-related side effects
E. Pentamidine
Rarely used now due to poor tolerability and effectiveness
3. Special Situations
HIV Co-infection: Needs stronger regimens, often with liposomal amphotericin B
Pregnancy: Liposomal amphotericin B is the safest option
PKDL (Post Kala-Azar Dermal Leishmaniasis): Requires prolonged therapy (SSG or miltefosine)
114
What is the duration and dosing of liposomal amphotericin B?
A single dose of 10 mg/kg or multiple doses totaling 20 mg/kg over several days, depending on regional protocols.
115
What are the adverse effects of amphotericin B?
Nephrotoxicity, hypokalemia, infusion-related fever, chills, hypotension, and phlebitis.
116
How is miltefosine administered?
Miltefosine is given orally for 28 days. It is contraindicated in pregnancy and should be taken with food to reduce GI side effects.
117
What are the complications of untreated visceral leishmaniasis?
Progressive cachexia, recurrent infections, bleeding, liver dysfunction, and death.
118
What is post-kala-azar dermal leishmaniasis (PKDL)?
A dermal complication that occurs months to years after treatment, presenting as macular, papular, or nodular skin lesions containing parasites.
119
What are differential diagnoses of kala-azar?
Malaria, typhoid fever, leukemia, lymphoma, tuberculosis, and brucellosis.
120
What is the role of nutritional support in kala-azar treatment?
Malnourished children need adequate nutritional rehabilitation as malnutrition worsens outcomes and delays recovery.
121
How is kala-azar prevented?
Vector control (insecticide spraying, bed nets), early diagnosis and treatment, reservoir control, and health education.
122
What are the indicators for hospitalization in kala-azar?
Severe anemia, high parasite load, co-infection (e.g., HIV), poor nutritional status, and signs of organ dysfunction.
123
What is measles and its causative agent?
Measles is a highly contagious viral disease caused by the measles virus, a single-stranded, negative-sense RNA virus of the Paramyxoviridae family.
124
How is measles transmitted?
Measles is spread via respiratory droplets and airborne particles. It is highly infectious, with a basic reproduction number (R0) of 12–18.
125
What is the incubation period of measles?
Typically 7–14 days from exposure to onset of fever, with rash appearing around day 14.
126
What are the classical clinical stages of measles?
1) Incubation; 2) Prodromal phase (fever, cough, coryza, conjunctivitis, Koplik spots); 3) Exanthem phase (maculopapular rash); 4) Recovery.
127
What are Koplik spots and their significance?
Small bluish-white lesions with a red halo on the buccal mucosa, pathognomonic for measles, appearing 1–2 days before the rash.
128
What is the typical progression of measles rash?
Maculopapular rash begins at the hairline/behind ears, spreads to the face, trunk, then extremities, often with confluence and fading in the same order.
129
What laboratory findings support measles diagnosis?
Leukopenia, relative lymphocytosis, elevated CRP, and positive measles IgM antibodies or PCR from nasopharyngeal secretions.
130
What is the WHO clinical case definition of measles?
Generalized maculopapular rash, fever, and at least one of the following: cough, coryza, or conjunctivitis.
131
What are the complications of measles in children?
Otitis media, pneumonia (most common cause of death), diarrhea, laryngotracheobronchitis, encephalitis, and subacute sclerosing panencephalitis (SSPE).
132
What is SSPE and when does it occur?
Subacute sclerosing panencephalitis is a fatal, delayed complication of measles occurring years after infection due to persistent viral infection in the CNS.
133
Which populations are at highest risk of severe measles?
Malnourished children, immunocompromised patients, infants, and those with vitamin A deficiency.
134
What is the role of vitamin A in measles?
Vitamin A reduces severity and mortality; WHO recommends supplementation for all children with measles (200,000 IU for ≥12 months, 100,000 IU for 6–11 months).
135
What is the treatment for measles?
Supportive care: hydration, antipyretics, nutritional support, and vitamin A. Antibiotics for secondary bacterial infections.
136
How is measles diagnosed in resource-limited settings?
Clinically based on rash, fever, and triad of cough, coryza, conjunctivitis; confirmed with IgM serology or PCR if available.
137
What is the measles case fatality rate (CFR)?
Globally, CFR ranges from 0.1% to 5%, but can exceed 10% in malnourished or unvaccinated populations.
138
How is measles prevented?
Vaccination with the live attenuated measles-containing vaccine (e.g., MMR or MR vaccine), first dose at 9–12 months, second at 15–18 months or school entry.
139
What are contraindications to measles vaccination?
Severe immunodeficiency, pregnancy, and previous anaphylaxis to vaccine components (e.g., gelatin, neomycin).
140
What is the significance of herd immunity in measles?
Herd immunity threshold is ~95%, meaning high population coverage is needed to prevent outbreaks.
141
What are the guidelines for post-exposure prophylaxis in measles?
Measles vaccine within 72 hours or immunoglobulin within 6 days for high-risk groups (infants, pregnant women, immunocompromised).
142
What is the global measles elimination strategy?
High vaccine coverage, surveillance, outbreak response, and supplemental immunization activities as per WHO/UNICEF goals.
143
What is tetanus and its causative organism?
Tetanus is a potentially fatal neurologic disease caused by Clostridium tetani, a gram-positive, spore-forming anaerobic bacterium that produces tetanospasmin toxin.
144
How does Clostridium tetani cause disease?
Spores enter through wounds and germinate under anaerobic conditions, producing tetanospasmin, which blocks inhibitory neurotransmitter release (GABA and glycine) at motor neuron terminals.
145
What are common modes of tetanus transmission?
Contaminated wounds, umbilical stump infections (neonatal tetanus), puncture injuries, burns, surgical procedures, and poor obstetric practices.
146
What are the clinical forms of tetanus?
Generalized tetanus (most common), localized tetanus, cephalic tetanus, and neonatal tetanus.
147
What are the cardinal features of generalized tetanus?
Trismus (lockjaw), risus sardonicus, opisthotonus, generalized muscle rigidity, and painful spasms often triggered by stimuli.
148
What is neonatal tetanus and how does it present?
Occurs in newborns, typically between 3–14 days of life, presenting with poor feeding, rigidity, spasms, and inability to suck, usually due to contaminated umbilical cord care.
149
How is tetanus diagnosed?
Tetanus is a clinical diagnosis based on characteristic symptoms; there are no definitive laboratory tests. Wound cultures are often negative.
150
What are differential diagnoses for tetanus?
Meningitis, dystonic cerebral palsy, hypocalcemic tetany, strychnine poisoning, and epilepsy.
151
What is the incubation period of tetanus?
Usually 3–21 days, but shorter incubation (<7 days) is associated with more severe disease.
152
What is the first step in tetanus management?
Ensure a quiet environment, supportive care (airway, hydration, nutrition), control of spasms, neutralization of unbound toxin, and eradication of bacteria.
153
What is the role of tetanus immunoglobulin (TIG)?
TIG is given intramuscularly (3000–6000 units in older children, 500 units in neonates) to neutralize circulating unbound toxin.
154
What antibiotics are used in tetanus treatment?
Metronidazole (preferred) or penicillin G to eradicate C. tetani. Avoid high-dose penicillin due to potential GABA antagonism.
155
What agents are used to control muscle spasms?
Benzodiazepines (e.g., diazepam, midazolam), baclofen, magnesium sulfate, or neuromuscular blockers in severe cases requiring ventilation.
156
What supportive measures are essential in tetanus?
Airway protection, sedation, control of spasms, nutritional support (NG feeding), temperature control, and intensive care monitoring.
157
What is the prognosis of tetanus in children?
Without treatment, mortality is high (>50%). With ICU support, prognosis improves, especially in older children. Neonatal tetanus has the highest mortality.
158
What is the role of vaccination in tetanus prevention?
Tetanus toxoid-containing vaccines (DTP/DTaP) are highly effective. A full primary series followed by booster doses provides long-term protection.
159
What is the DTP vaccine schedule in children?
Three primary doses at 6, 10, and 14 weeks, followed by boosters at 15–18 months and 4–6 years. Tetanus boosters every 10 years thereafter.
160
How is post-exposure prophylaxis (PEP) for tetanus managed?
Depends on wound type and immunization history. Clean wounds need a booster if >10 years since last dose; dirty wounds need TIG if not fully vaccinated.
161
What are the global targets for tetanus elimination?
Neonatal tetanus elimination is defined as <1 case per 1000 live births per district/year. WHO strategies include maternal immunization and clean delivery practices.
162
What is the role of maternal immunization in neonatal tetanus prevention?
Two doses of tetanus toxoid during pregnancy protect both mother and newborn, reducing neonatal tetanus risk by up to 94%.
163
What is rabies and what causes it?
Rabies is an acute, progressive viral encephalitis caused by the rabies virus, a neurotropic RNA virus in the Lyssavirus genus of the Rhabdoviridae family.
164
How is rabies transmitted?
Through the saliva of infected animals via bites, scratches, or licking of mucous membranes or broken skin. Dogs are the primary source in endemic countries.
165
What animals are common reservoirs of rabies?
Dogs (most common globally), bats (notably in the Americas), raccoons, skunks, foxes, and mongooses.
166
What is the incubation period of rabies?
Typically 1–3 months but can range from a few days to several years, depending on the site, severity, and viral load.
167
What is the pathophysiology of rabies?
The virus replicates in muscle at the site of entry, then enters peripheral nerves via acetylcholine receptors and travels retrogradely to the CNS, leading to encephalitis.
168
What are the clinical forms of rabies?
Furious (encephalitic) rabies and paralytic (dumb) rabies. Furious rabies is more common and presents with hyperactivity and hydrophobia.
169
What are the hallmark signs of furious rabies?
Hydrophobia (painful spasms triggered by attempts to swallow liquids), aerophobia, agitation, confusion, hallucinations, and autonomic instability.
170
What is paralytic (dumb) rabies?
A less common form presenting with ascending paralysis, confusion, coma, and eventual respiratory failure, often misdiagnosed as Guillain-Barré syndrome.
171
How is rabies diagnosed clinically?
Rabies should be suspected in any acute progressive encephalitis, particularly following animal bites. Early symptoms include fever, malaise, headache, and paresthesia at the bite site.
172
How is laboratory diagnosis of rabies made?
Detection of viral RNA by RT-PCR from saliva, CSF, or nuchal skin biopsy; detection of antibodies in CSF or serum in unvaccinated patients.
173
What is the prognosis of symptomatic rabies?
Almost universally fatal once symptoms appear, despite intensive supportive care.
174
What is the Milwaukee protocol?
An experimental treatment involving induced coma and antiviral therapy. Limited success and not recommended routinely.
175
What is the cornerstone of rabies prevention?
Post-exposure prophylaxis (PEP) with thorough wound cleaning, rabies immunoglobulin (RIG), and vaccination.
176
What are the WHO categories of rabies exposure?
Category I: touch/lick on intact skin (no PEP); Category II: minor scratches/nibbles (vaccine); Category III: transdermal bites, mucosal exposure (RIG + vaccine).
177
What is the rabies PEP vaccine schedule?
For unvaccinated individuals: intramuscular regimen on days 0, 3, 7, and 14. Immunocompromised patients get a fifth dose on day 28.
178
What is the role of rabies immunoglobulin (RIG)?
RIG provides immediate passive immunity and should be infiltrated around the wound site in Category III exposures, ideally within 7 days of vaccination.
179
What are the types of rabies vaccines?
Cell culture-based vaccines such as human diploid cell vaccine (HDCV) and purified chick embryo cell vaccine (PCECV) are used for pre- and post-exposure prophylaxis.
180
How is pre-exposure prophylaxis for rabies given?
Recommended for high-risk groups (veterinarians, animal handlers): 3 doses on days 0, 7, and 21/28.
181
What is the importance of wound care in rabies PEP?
Immediate and thorough washing with soap and water for 15 minutes significantly reduces viral load and transmission risk.
182
What are the global rabies elimination strategies?
Mass dog vaccination, improved access to PEP, public education, and strengthened surveillance systems per WHO's goal to eliminate dog-mediated rabies deaths by 2030.
183
What is brucellosis and its causative agents?
Brucellosis is a zoonotic bacterial infection caused by Brucella species—primarily B. melitensis, B. abortus, B. suis, and B. canis.
184
How is brucellosis transmitted to humans?
Through direct contact with infected animals or consumption of unpasteurized dairy products. Occupational exposure and inhalation in labs are also possible.
185
Which Brucella species is most pathogenic to humans?
Brucella melitensis, associated with sheep and goats, is the most virulent and common cause of human brucellosis.
186
What is the pathophysiology of brucellosis?
Brucellae enter through mucosa or broken skin, are phagocytosed by macrophages, and multiply intracellularly, leading to systemic dissemination and granulomatous inflammation.
187
What is the incubation period of brucellosis?
Typically 1–3 weeks, but can range from 5 days to several months.
188
What are the typical clinical features of acute brucellosis?
Fever, malaise, night sweats (often with a musty odor), arthralgia, hepatosplenomegaly, lymphadenopathy, and weight loss.
189
How does chronic brucellosis present?
Persistent or relapsing symptoms lasting >1 year, including fatigue, low-grade fever, arthritis, and depression.
190
What are focal complications of brucellosis in children?
Osteoarticular involvement (most common), neurobrucellosis, endocarditis, orchitis, and hepatitis.
191
What are the features of osteoarticular brucellosis?
Arthritis, sacroiliitis, spondylitis, or osteomyelitis. Hip and knee joints are commonly involved in children.
192
What are neurological manifestations of brucellosis?
Neurobrucellosis may present with meningitis, encephalitis, cranial nerve palsies, or psychiatric symptoms.
193
How is brucellosis diagnosed?
Serologic tests (e.g., standard agglutination test, SAT; ELISA), blood cultures, and bone marrow cultures are diagnostic. PCR may aid in confirmation.
194
What is the role of blood cultures in brucellosis?
Blood cultures can be positive in 40–70% of cases, especially during the acute phase. Bone marrow cultures have higher sensitivity.
195
What is the standard treatment for brucellosis in children?
Combination of rifampicin + doxycycline for ≥6 weeks. In children <8 years or pregnant patients, doxycycline is replaced with cotrimoxazole.
196
What is the treatment for complicated brucellosis (e.g., neurobrucellosis)?
Triple therapy with rifampicin, doxycycline, and an aminoglycoside (e.g., streptomycin or gentamicin) for an extended duration.
197
What is the duration of therapy in osteoarticular brucellosis?
Typically 8–12 weeks or longer, depending on the clinical response and severity.
198
How is pediatric brucellosis different from adult presentation?
Children often have a more acute onset with fever and musculoskeletal symptoms, but neurobrucellosis is rarer.
199
What are the common lab findings in brucellosis?
Anemia, leukopenia or leukocytosis, thrombocytopenia, elevated ESR and CRP, and mild transaminitis.
200
How is brucellosis prevented?
Pasteurization of milk, proper cooking of meat, vaccination of animals, use of protective gear by workers, and control of animal movement.
201
What is the role of the Brucella vaccine?
Animal vaccination (e.g., Rev-1 for B. melitensis) is key in controlling disease in endemic regions. No human vaccine is currently available.
202
What are the differential diagnoses of brucellosis?
Tuberculosis, typhoid fever, malaria, endocarditis, systemic lupus erythematosus, and lymphoma.
203
What are rickettsial infections and their causative organisms?
Rickettsial infections are caused by obligate intracellular, gram-negative bacteria of the genera Rickettsia, Orientia, Ehrlichia, and Anaplasma.
204
What are the major types of rickettsial infections in children?
Spotted fever group (e.g., Rocky Mountain spotted fever), typhus group (e.g., epidemic typhus), and scrub typhus (caused by Orientia tsutsugamushi).
205
What is scrub typhus and where is it endemic?
Scrub typhus is a zoonotic rickettsial disease endemic in the 'tsutsugamushi triangle'—parts of Asia-Pacific, caused by Orientia tsutsugamushi.
206
How is scrub typhus transmitted?
Through the bite of infected larval trombiculid mites (chiggers) found in grassy or bushy areas.
207
What are the clinical features of rickettsial infections?
Acute febrile illness with fever, headache, myalgia, rash, lymphadenopathy, hepatosplenomegaly, and eschar (especially in scrub typhus).
208
What is an eschar and its significance?
A painless black necrotic scab at the site of chigger bite, highly suggestive of scrub typhus but may not always be present.
209
What are the complications of untreated rickettsial infections?
Meningoencephalitis, ARDS, hepatitis, acute kidney injury, myocarditis, shock, and death.
210
What laboratory findings are common in rickettsial infections?
Leukopenia or leukocytosis, thrombocytopenia, elevated transaminases, hyponatremia, and elevated CRP/ESR.
211
How is rickettsial infection diagnosed?
Clinically in endemic areas. Confirmatory tests include serology (IFA, ELISA), PCR, or Weil-Felix test (limited sensitivity).
212
What is the Weil-Felix test and its role?
An agglutination test using Proteus OX strains; it's outdated due to poor sensitivity/specificity but still used in resource-limited settings.
213
What is the treatment of choice for rickettsial infections in children?
Doxycycline is first-line even in children under 8 years; it is safe and effective when used for short durations.
214
What are alternative treatments for rickettsial infections?
Azithromycin is used in doxycycline-allergic or pregnant patients, and chloramphenicol may be used in some severe or resistant cases.
215
What is the typical response to treatment in rickettsial infections?
Rapid defervescence within 48 hours of doxycycline is a hallmark of effective treatment.
216
What is the epidemiological importance of rickettsial infections?
Often underdiagnosed, they are important differential diagnoses in febrile illness in endemic tropical regions with nonspecific symptoms.
217
What is Rocky Mountain spotted fever and how does it present?
Caused by Rickettsia rickettsii, it presents with high fever, headache, rash (starts on wrists/ankles and spreads centrally), and rapid progression to multiorgan dysfunction.
218
How does murine typhus differ from epidemic typhus?
Murine typhus (R. typhi) is transmitted by fleas and milder, while epidemic typhus (R. prowazekii) is louse-borne and more severe.
219
What CNS manifestations occur in rickettsial infections?
Confusion, seizures, meningitis, and encephalitis can occur, particularly in severe or untreated cases.
220
What are predictors of severe disease in rickettsial infections?
Delayed treatment, absence of eschar, CNS involvement, elevated liver enzymes, and thrombocytopenia.
221
How can rickettsial infections be prevented?
Avoiding mite-infested areas, wearing protective clothing, use of repellents (DEET), and environmental control.
222
Why is early empirical therapy critical in rickettsial diseases?
Delayed antibiotic initiation increases morbidity and mortality; treatment should not await confirmatory test results in suspected cases.
223
What is HIV and how is it transmitted in children?
HIV (Human Immunodeficiency Virus) is a retrovirus that infects CD4+ T cells. In children, transmission occurs perinatally (in utero, intrapartum, or via breastfeeding), or less commonly through contaminated blood or sexual abuse.
224
What are the types of HIV?
HIV-1 is the most common worldwide, while HIV-2 is less transmissible and found primarily in West Africa.
225
What are the risk factors for mother-to-child HIV transmission?
High maternal viral load, lack of antiretroviral therapy (ART), prolonged rupture of membranes, vaginal delivery, breastfeeding, and co-infections (e.g., STIs).
226
What is the role of PMTCT in reducing HIV transmission?
Prevention of mother-to-child transmission (PMTCT) involves antenatal HIV screening, maternal ART, cesarean delivery when indicated, and neonatal prophylaxis.
227
When should HIV testing be done in exposed infants?
PCR (HIV DNA or RNA) testing is done at birth, 6 weeks, and 3–6 months. Antibody testing is unreliable before 18 months due to maternal antibodies.
228
What is the diagnostic test for HIV in infants <18 months?
HIV DNA PCR or HIV RNA PCR is used. Two positive PCRs confirm the diagnosis.
229
What are early signs of HIV in children?
Failure to thrive, recurrent oral thrush, persistent lymphadenopathy, hepatosplenomegaly, chronic diarrhea, and frequent respiratory infections.
230
What are AIDS-defining illnesses in children?
Pneumocystis pneumonia, esophageal candidiasis, chronic herpes simplex, CMV, MAC, Kaposi’s sarcoma, and recurrent bacterial infections.
231
What are WHO clinical stages of pediatric HIV?
Stage I: asymptomatic; Stage II: mild symptoms; Stage III: moderate (e.g., severe malnutrition, chronic diarrhea); Stage IV: severe or AIDS-defining conditions.
232
What are the goals of antiretroviral therapy (ART)?
Suppress viral replication, restore immune function (CD4 recovery), reduce morbidity and mortality, and prevent transmission.
233
What is the standard first-line ART regimen in children?
Typically includes two NRTIs (e.g., abacavir + lamivudine) and one NNRTI or integrase inhibitor (e.g., dolutegravir).
234
What is the role of cotrimoxazole prophylaxis in pediatric HIV?
Cotrimoxazole is given to prevent Pneumocystis jirovecii pneumonia and other opportunistic infections, especially in infants and those with low CD4 counts.
235
What vaccines are contraindicated in HIV-infected children?
Live vaccines (e.g., BCG, OPV, MMR, varicella) are contraindicated in severely immunosuppressed children, but may be used if CD4 counts are adequate.
236
How is HIV monitored in children on ART?
Viral load is the most sensitive indicator of treatment efficacy. CD4 counts are used to assess immune recovery.
237
What are side effects of ART in children?
Anemia, hepatotoxicity, lipodystrophy, hypersensitivity reactions, lactic acidosis, and GI symptoms.
238
What is immune reconstitution inflammatory syndrome (IRIS)?
A paradoxical worsening of preexisting infections due to immune recovery following ART initiation.
239
What are indicators of ART failure in children?
Persistent high viral load (>1000 copies/mL), declining CD4 count, or clinical progression despite ART.
240
How is adherence to ART promoted in children?
Caregiver education, simplified regimens, palatable formulations, and routine counseling improve adherence.
241
What psychosocial issues affect HIV-infected children?
Stigma, depression, poor school attendance, orphanhood, and delayed disclosure of diagnosis are common challenges.
242
What is the long-term prognosis of children with HIV on ART?
With early diagnosis and effective ART, children can achieve normal growth, development, and life expectancy.
243
What is poliomyelitis and what causes it?
Poliomyelitis (polio) is a highly infectious viral disease caused by poliovirus, a single-stranded RNA virus belonging to the Enterovirus genus.
244
How is poliovirus transmitted?
Primarily via the fecal-oral route; less commonly via oral-oral transmission through respiratory droplets.
245
What are the types of poliovirus?
There are three serotypes of wild poliovirus: type 1, type 2 (eradicated), and type 3 (eradicated as of 2019). Type 1 remains endemic in a few countries.
246
What are the clinical forms of polio?
1) Asymptomatic (90–95%), 2) Abortive polio (minor illness), 3) Non-paralytic aseptic meningitis, 4) Paralytic polio (flaccid paralysis).
247
What is the pathophysiology of paralytic polio?
The virus invades the CNS and selectively destroys anterior horn cells in the spinal cord, leading to motor neuron death and flaccid paralysis.
248
What are the characteristics of paralytic poliomyelitis?
Acute onset of asymmetric, flaccid paralysis without sensory loss, often preceded by fever, malaise, and myalgia.
249
What is bulbar poliomyelitis?
A severe form where the virus affects the medulla and cranial nerves, leading to respiratory failure, dysphagia, and cranial nerve palsies.
250
What are risk factors for developing paralytic polio?
Low immunity, lack of vaccination, physical trauma, or injections during the viremic phase.
251
How is polio diagnosed?
Clinical diagnosis supported by isolation of poliovirus from stool or throat swabs. CSF shows lymphocytic pleocytosis and mildly elevated protein.
252
What is the differential diagnosis of acute flaccid paralysis (AFP)?
Guillain-Barré syndrome, transverse myelitis, traumatic neuritis, enterovirus D68, and spinal cord tumors.
253
What are the WHO criteria for AFP surveillance?
All children under 15 years with new onset flaccid paralysis should be investigated for polio. Two stool samples within 14 days are required.
254
How is polio treated?
There is no antiviral therapy. Management is supportive: bed rest, physical therapy, respiratory support for bulbar cases, and prevention of deformities.
255
What is the prognosis of paralytic polio?
Some children recover partially or fully; others may have permanent disability. Bulbar and respiratory forms have higher mortality.
256
What is post-polio syndrome?
A condition that appears decades after initial infection, characterized by new muscle weakness, fatigue, and pain in previously affected muscles.
257
What are the types of polio vaccines?
1) Inactivated polio vaccine (IPV), given IM; 2) Oral polio vaccine (OPV), a live attenuated vaccine.
258
What are the advantages and disadvantages of OPV?
Advantages: mucosal immunity, herd protection. Disadvantages: rare risk of vaccine-associated paralytic polio (VAPP) and circulating vaccine-derived poliovirus (cVDPV).
259
What is the polio vaccination schedule in children?
WHO recommends at least 3 doses of OPV and 1 dose of IPV. National schedules vary, often at 6, 10, 14 weeks and booster at 15–18 months.
260
What is cVDPV and how does it arise?
Circulating vaccine-derived poliovirus (cVDPV) arises when the attenuated virus in OPV mutates and regains neurovirulence in under-immunized populations.
261
What are the global strategies for polio eradication?
Mass vaccination campaigns, routine immunization, AFP surveillance, rapid outbreak response, and containment of poliovirus in labs.
262
What is the current status of global polio eradication?
Wild poliovirus remains endemic only in Afghanistan and Pakistan. All WHO regions except these are certified polio-free.
263
What are the main types of viral hepatitis affecting children?
Hepatitis A virus (HAV), hepatitis B virus (HBV), and hepatitis C virus (HCV) are the most relevant in pediatric populations.
264
What is the mode of transmission of hepatitis A?
Fecal-oral route, typically through contaminated food, water, or close personal contact in areas with poor sanitation.
265
What is the typical clinical presentation of hepatitis A in children?
Fever, malaise, anorexia, nausea, vomiting, abdominal pain, followed by jaundice and dark urine. Many cases in young children are asymptomatic.
266
How is hepatitis A diagnosed?
Detection of serum anti-HAV IgM antibodies confirms acute infection. IgG indicates past infection or vaccination.
267
What is the management of hepatitis A in children?
Supportive care only, as the disease is self-limited. No antiviral treatment is necessary.
268
What is the role of the hepatitis A vaccine?
Inactivated vaccine given in 2 doses at 12 months and 6–18 months later. Highly effective in preventing HAV infection.
269
How is hepatitis B transmitted in children?
Perinatally from infected mothers, horizontal transmission via contact with infected blood or body fluids, and through unsafe medical practices.
270
What are the clinical features of acute hepatitis B?
Similar to HAV: fever, jaundice, anorexia, nausea, and vomiting. Many children are asymptomatic or have mild illness.
271
What is the risk of chronicity in HBV infection?
90% in perinatally infected infants, 20–50% in children <5 years, and <5% in adults.
272
What are the complications of chronic hepatitis B?
Cirrhosis, hepatocellular carcinoma, and liver failure later in life.
273
How is hepatitis B diagnosed?
Detection of HBsAg and anti-HBc IgM for acute infection; HBsAg persistence >6 months indicates chronic infection.
274
What is the treatment for chronic hepatitis B in children?
Indicated in selected cases with elevated ALT and high HBV DNA. Options include interferon-alpha and nucleos(t)ide analogs like entecavir or tenofovir.
275
How is HBV prevented in children?
Universal vaccination at birth, followed by completion of the vaccine series. Hepatitis B immunoglobulin (HBIG) is given to infants born to HBsAg-positive mothers.
276
What is the hepatitis B vaccination schedule?
Typically at birth, 6 weeks, and 14 weeks, or birth, 1 month, and 6 months depending on national guidelines.
277
How is hepatitis C transmitted in children?
Primarily via perinatal transmission. Less commonly through transfusions, unsafe injections, or rarely sexual abuse.
278
What is the clinical presentation of hepatitis C in children?
Often asymptomatic. When symptomatic, may include fatigue, mild ALT elevation, and in rare cases, jaundice.
279
How is HCV diagnosed in children?
Anti-HCV antibodies (after 18 months) and HCV RNA PCR (after 2–3 months of age) for early detection.
280
What is the treatment for chronic hepatitis C in children?
Direct-acting antivirals (DAAs) such as sofosbuvir/ledipasvir or glecaprevir/pibrentasvir are approved for children >3 years.
281
What are the goals of HCV treatment in children?
Achieve sustained virologic response (SVR), prevent progression to cirrhosis, and reduce the risk of hepatocellular carcinoma.
282
What preventive strategies exist for HCV in children?
Screening of blood products, safe medical practices, and infection control. No vaccine currently exists for HCV.
283
What is diphtheria and what causes it?
Diphtheria is an acute bacterial infection caused by Corynebacterium diphtheriae, a gram-positive bacillus that produces diphtheria toxin.
284
What are the major forms of diphtheria in children?
Respiratory diphtheria (pharyngeal, laryngeal, nasal) and cutaneous diphtheria.
285
What is the pathogenesis of diphtheria toxin?
The exotoxin inhibits protein synthesis by inactivating elongation factor-2 (EF-2), leading to cell death and pseudomembrane formation.
286
What is the hallmark of respiratory diphtheria?
Grayish-white pseudomembrane over the tonsils, pharynx, or larynx that bleeds on attempted removal.
287
What are systemic complications of diphtheria toxin?
Myocarditis, arrhythmias, heart block, neuritis (cranial and peripheral nerves), and renal failure.
288
What are symptoms of respiratory diphtheria?
Fever, sore throat, dysphagia, hoarseness, stridor, cervical lymphadenopathy ('bull neck' appearance), and pseudomembrane formation.
289
What is the incubation period of diphtheria?
Typically 2–5 days post-exposure.
290
How is diphtheria diagnosed?
Clinical suspicion based on pseudomembrane and systemic toxicity. Confirmed by culture of C. diphtheriae and toxin testing (Elek test or PCR).
291
What is the treatment for diphtheria?
Administer diphtheria antitoxin (DAT) immediately without waiting for lab confirmation, along with antibiotics (erythromycin or penicillin).
292
What is the role of the diphtheria antitoxin?
Neutralizes circulating (unbound) toxin. Does not reverse effects of already bound toxin.
293
What antibiotics are used in diphtheria?
Intramuscular penicillin or oral erythromycin for 14 days. Antibiotics also reduce carriage.
294
When is isolation indicated for diphtheria?
Droplet and contact precautions are necessary until 2 consecutive negative cultures are obtained post-antibiotics.
295
What are the complications of diphtheria myocarditis?
Arrhythmias, congestive heart failure, and sudden death. It is the leading cause of death in diphtheria.
296
What neurological complications are seen in diphtheria?
Palatal paralysis, cranial nerve deficits (especially CN IX, X), limb weakness, and respiratory muscle paralysis.
297
What is cutaneous diphtheria?
Skin ulcers with grayish membrane, usually less toxic than respiratory form. Common in tropical climates.
298
What are differential diagnoses of diphtheria?
Streptococcal pharyngitis, infectious mononucleosis, Vincent angina, candidiasis, and epiglottitis.
299
What is the diphtheria vaccination schedule in children?
DTP (diphtheria, tetanus, pertussis) at 6, 10, and 14 weeks, with boosters at 15–18 months and 4–6 years.
300
What is the role of diphtheria toxoid in prevention?
The vaccine is a formalin-inactivated diphtheria toxoid that induces protective antibody response.
301
What is the case-fatality rate of diphtheria?
Ranges from 5% to 10% overall, but can exceed 20% in young children or with delayed treatment.
302
How is diphtheria carriage managed in asymptomatic contacts?
Erythromycin for 7–10 days or single-dose benzathine penicillin, plus booster vaccination if needed.
303
What is pertussis and what causes it?
Pertussis, or whooping cough, is a highly contagious respiratory illness caused by Bordetella pertussis, a gram-negative coccobacillus.
304
What are the stages of pertussis infection?
1) Catarrhal stage (1–2 weeks): mild URTI symptoms. 2) Paroxysmal stage (2–6 weeks): severe coughing fits with inspiratory 'whoop'. 3) Convalescent stage (weeks to months): gradual recovery.
305
What is the typical presentation in the catarrhal stage?
Nasal congestion, rhinorrhea, low-grade fever, and mild cough—often mistaken for a common cold.
306
What characterizes the paroxysmal stage of pertussis?
Repeated intense coughing spells followed by a high-pitched inspiratory 'whoop' and post-tussive vomiting or apnea in infants.
307
What are complications of pertussis in infants?
Apnea, hypoxia, pneumonia, seizures, encephalopathy, and death, especially in infants <6 months.
308
What is the pathophysiology of pertussis?
Pertussis toxin and other virulence factors disrupt mucociliary clearance, impair immune response, and cause lymphocytosis.
309
How is pertussis diagnosed?
Nasopharyngeal swab for PCR (preferred), culture (gold standard but less sensitive), or serology (in older children and adults).
310
What is the role of WBC count in pertussis?
Marked lymphocytosis is characteristic, especially in infants, and may aid diagnosis in settings lacking PCR.
311
What are differential diagnoses for pertussis?
Bronchiolitis, viral croup, asthma, GERD, foreign body aspiration, and other bacterial pneumonias.
312
What is the first-line antibiotic treatment for pertussis?
Macrolides (azithromycin, clarithromycin, erythromycin). Azithromycin is preferred due to fewer side effects.
313
When is antibiotic therapy most effective in pertussis?
Most effective during the catarrhal stage. It reduces transmission and duration if started early.
314
What is the role of post-exposure prophylaxis for pertussis?
Close contacts of confirmed cases should receive macrolide prophylaxis, especially infants and high-risk individuals.
315
What is the pertussis vaccination schedule?
DTaP at 6, 10, and 14 weeks with boosters at 15–18 months and 4–6 years. Tdap booster in adolescence and during every pregnancy.
316
What are acellular versus whole-cell pertussis vaccines?
Acellular vaccines (DTaP/Tdap) contain purified components and have fewer side effects than whole-cell vaccines but possibly less durable immunity.
317
Why is pertussis resurgence observed despite vaccination?
Waning immunity from acellular vaccines, suboptimal booster coverage, and asymptomatic transmission by vaccinated individuals.
318
What supportive care is needed in severe pertussis?
Hospitalization, monitoring for apnea/hypoxia, oxygen therapy, suctioning, nutritional support, and in rare cases, intubation.
319
What are risk factors for severe pertussis in children?
Age <6 months, unvaccinated status, premature birth, co-infections, and underlying cardiorespiratory disease.
320
How is pertussis different in adolescents and adults?
They may present with prolonged paroxysmal cough without 'whoop'; often a source of infant infection.
321
What is the significance of maternal vaccination for pertussis?
Tdap during pregnancy (preferably in the third trimester) protects infants via transplacental antibody transfer.
322
What is the global burden and prevention strategy for pertussis?
Despite vaccines, pertussis remains endemic globally. Strategies include immunization coverage, booster doses, and maternal vaccination.
323
What is CMV and how is it transmitted?
Cytomegalovirus (CMV) is a herpesvirus transmitted via saliva, urine, breast milk, blood transfusion, organ transplantation, and vertically from mother to fetus.
324
What are the clinical features of congenital CMV infection?
Jaundice, hepatosplenomegaly, microcephaly, periventricular calcifications, chorioretinitis, thrombocytopenia, sensorineural hearing loss, and developmental delay.
325
How is congenital CMV diagnosed?
Detection of CMV DNA in urine or saliva within the first 3 weeks of life confirms congenital infection.
326
What are long-term sequelae of congenital CMV?
Sensorineural hearing loss, intellectual disability, cerebral palsy, epilepsy, and visual impairment.
327
What is the treatment for symptomatic congenital CMV?
Oral valganciclovir for 6 months is the standard; IV ganciclovir is used in severe cases.
328
How does postnatal CMV infection present in immunocompetent children?
Often asymptomatic or mild mononucleosis-like illness with fever, lymphadenopathy, and fatigue.
329
What are CMV complications in immunocompromised children?
Pneumonitis, hepatitis, retinitis, gastroenteritis, and bone marrow suppression.
330
How is CMV infection diagnosed in older children?
CMV IgM and IgG serology, CMV PCR (blood), or antigenemia assay.
331
What is Epstein-Barr Virus (EBV) and its mode of transmission?
EBV is a herpesvirus transmitted via saliva. It causes infectious mononucleosis and is associated with lymphoproliferative disorders.
332
What are clinical features of infectious mononucleosis (IM)?
Fever, sore throat, generalized lymphadenopathy, hepatosplenomegaly, malaise, and sometimes rash.
333
What is the pathophysiology of EBV infection?
EBV infects B cells via the CD21 receptor, causing polyclonal B-cell activation and proliferation.
334
How is EBV infection diagnosed?
Heterophile antibody (Monospot) test, EBV-specific IgM/IgG, and PCR in immunocompromised patients.
335
What are atypical lymphocytes in EBV infection?
Reactive cytotoxic CD8+ T cells seen on blood smear, supporting the diagnosis of infectious mononucleosis.
336
What complications are associated with EBV?
Splenic rupture, airway obstruction, autoimmune hemolytic anemia, thrombocytopenia, and neurological complications like meningitis.
337
What is the management of infectious mononucleosis?
Supportive care: hydration, rest, antipyretics. Avoid contact sports for ≥4 weeks due to splenomegaly.
338
What is the role of corticosteroids in EBV infection?
Used in severe complications such as airway obstruction, hemolytic anemia, or thrombocytopenia.
339
What are EBV-associated malignancies?
Burkitt lymphoma, Hodgkin lymphoma, nasopharyngeal carcinoma, and post-transplant lymphoproliferative disorder (PTLD).
340
What is PTLD and its association with EBV?
Post-transplant lymphoproliferative disorder is a potentially fatal complication in immunosuppressed transplant recipients due to EBV-driven B-cell proliferation.
341
How can CMV be prevented in high-risk populations?
Hand hygiene, screening blood/tissue donors, using CMV-negative or leukoreduced products, and prophylactic antivirals in transplant patients.
342
How is EBV managed in immunocompromised children?
Reduction of immunosuppression, rituximab, and antivirals in PTLD or reactivation settings.
343
What does TORCH stand for in congenital infections?
TORCH stands for Toxoplasmosis, Other (including syphilis, varicella-zoster, parvovirus B19), Rubella, Cytomegalovirus (CMV), and Herpes simplex virus (HSV).
344
What are common features of congenital TORCH infections?
Intrauterine growth restriction, microcephaly, hepatosplenomegaly, jaundice, rash, chorioretinitis, and neurodevelopmental delay.
345
How is congenital toxoplasmosis transmitted?
Transplacentally from a mother infected during pregnancy, especially with primary Toxoplasma gondii infection.
346
What are clinical features of congenital toxoplasmosis?
Chorioretinitis, hydrocephalus, intracranial calcifications (diffuse), seizures, and developmental delay.
347
How is congenital toxoplasmosis diagnosed?
Detection of Toxoplasma IgM/IgA in the infant, PCR from amniotic fluid, or serologic testing in mother-infant pairs.
348
What is the treatment of congenital toxoplasmosis?
Pyrimethamine + sulfadiazine + folinic acid for 12 months.
349
What is the most common finding in congenital rubella syndrome (CRS)?
Sensorineural hearing loss is the most common feature, followed by cataracts, congenital heart defects (PDA, pulmonary artery stenosis), and blueberry muffin rash.
350
What is the critical period of risk for CRS?
First trimester of pregnancy carries the highest risk for severe fetal anomalies.
351
How is congenital rubella diagnosed?
Detection of rubella-specific IgM in infant serum or persistent IgG beyond 6 months, or PCR of rubella virus.
352
What is the prevention of rubella infection?
MMR vaccination of women before pregnancy and universal childhood vaccination.
353
What are features of congenital CMV infection?
Sensorineural hearing loss, periventricular calcifications, microcephaly, hepatosplenomegaly, thrombocytopenia, and chorioretinitis.
354
How is congenital CMV differentiated from rubella?
CMV has periventricular calcifications and no heart defects; rubella has diffuse calcifications and PDA.
355
What are signs of congenital HSV infection?
Vesicular skin lesions, seizures, encephalitis, hepatitis, and disseminated sepsis-like illness.
356
How is neonatal HSV diagnosed?
PCR testing of CSF, vesicle swabs, and blood. Tzanck smear may show multinucleated giant cells.
357
What is the treatment for neonatal HSV?
IV acyclovir for 14–21 days, depending on severity and CNS involvement.
358
What is the 'blueberry muffin' rash and its significance?
It refers to dermal extramedullary hematopoiesis seen in congenital infections like rubella and CMV.
359
What are features of congenital syphilis?
Snuffles (bloody nasal discharge), rash, hepatosplenomegaly, periostitis, Hutchinson teeth, saddle nose, and interstitial keratitis.
360
How is congenital syphilis diagnosed?
Non-treponemal (VDRL/RPR) and treponemal (FTA-ABS) tests in infant and maternal serum, and CSF evaluation.
361
What is the treatment for congenital syphilis?
IV penicillin G for 10–14 days based on clinical findings and CSF involvement.
362
How can TORCH infections be prevented?
Prenatal screening, maternal immunization (rubella, varicella), avoidance of undercooked meat and cat litter (toxoplasmosis), and safe maternal-infant care.
363
What is varicella and what causes it?
Varicella, or chickenpox, is a primary infection caused by the varicella-zoster virus (VZV), a herpesvirus.
364
How is varicella transmitted?
Through respiratory droplets and direct contact with vesicular fluid. It is highly contagious.
365
What is the incubation period for varicella?
Typically 10–21 days, with most children developing symptoms around day 14.
366
What are the clinical features of varicella?
Fever, malaise, and a pruritic rash that progresses from macules to papules to vesicles and crusts, often appearing in crops.
367
What is the 'dew drop on a rose petal' appearance?
Describes the classic varicella vesicles with clear fluid on an erythematous base.
368
What are complications of varicella in children?
Secondary bacterial infections (e.g., impetigo), pneumonia, cerebellitis, encephalitis, and thrombocytopenia.
369
What neurologic complication is associated with varicella?
Acute cerebellar ataxia is the most common CNS complication, typically occurring in the recovery phase.
370
How is varicella diagnosed?
Primarily clinical; PCR of vesicle fluid or direct fluorescent antibody testing can confirm diagnosis.
371
What is the management of uncomplicated varicella?
Supportive care: antipyretics (avoid aspirin), antihistamines, skin care, and hydration.
372
When is antiviral therapy indicated in varicella?
For immunocompromised children, adolescents, chronic skin/lung disease, or moderate-to-severe disease: acyclovir or valacyclovir.
373
What is congenital varicella syndrome?
Occurs when maternal infection happens during the first 20 weeks; features include limb hypoplasia, cutaneous scars, eye defects, and neurologic impairment.
374
What is neonatal varicella?
Occurs when maternal varicella is contracted 5 days before or 2 days after delivery; can cause severe disseminated disease in neonates.
375
How is neonatal varicella managed?
IV acyclovir and varicella-zoster immune globulin (VZIG) if exposed within the peripartum window.
376
What is herpes zoster (shingles)?
Reactivation of latent VZV from sensory ganglia causing painful dermatomal vesicular rash.
377
Can children develop herpes zoster?
Yes, especially if infected with varicella at a young age or immunocompromised.
378
What is the role of varicella vaccination?
Live attenuated vaccine given at 12–15 months and 4–6 years. Reduces incidence and severity of varicella.
379
What are the contraindications to varicella vaccine?
Severe immunodeficiency, pregnancy, or allergy to gelatin/neomycin.
380
What is post-exposure prophylaxis for varicella?
Varicella vaccine within 3–5 days or VZIG for high-risk individuals if vaccine is contraindicated.
381
How is VZV infection managed in immunocompromised children?
Hospitalization, IV acyclovir, and strict isolation. Consider VZIG for exposure.
382
What precautions should be used for hospitalized children with varicella?
Airborne and contact isolation until all lesions have crusted over.
383
What is Parvovirus B19 and what does it cause?
Parvovirus B19 is a single-stranded DNA virus that causes erythema infectiosum (fifth disease) in children.
384
How is Parvovirus B19 transmitted?
Via respiratory droplets, blood products, and transplacental transmission.
385
What are the classic features of erythema infectiosum?
Slapped cheek rash on the face, followed by a lacy, reticular rash on the trunk and limbs. Often accompanied by low-grade fever.
386
What is the incubation period of Parvovirus B19?
Typically 4 to 14 days, but rash may appear up to 21 days after exposure.
387
What are the hematological effects of Parvovirus B19?
Transient aplastic crisis in children with hemolytic anemias (e.g., sickle cell disease) and pancytopenia in immunocompromised patients.
388
What are the manifestations in immunocompromised children?
Chronic pure red cell aplasia, persistent anemia, and reticulocytopenia.
389
What is the effect of Parvovirus B19 in pregnancy?
Intrauterine infection can cause fetal hydrops, miscarriage, and severe anemia.
390
How is Parvovirus B19 diagnosed?
Detection of IgM antibodies (acute infection), PCR for viral DNA (especially in immunocompromised), or bone marrow biopsy.
391
What is the treatment of uncomplicated erythema infectiosum?
Supportive care with antipyretics, fluids, and rest. Most children recover without complications.
392
What is the treatment for transient aplastic crisis?
Blood transfusions may be needed. IVIG in immunocompromised children.
393
What is the role of IVIG in Parvovirus B19 infection?
IVIG is used to treat chronic B19 infection in immunocompromised children and severe anemia.
394
What is the differential diagnosis of the slapped cheek rash?
Rubella, measles, enteroviral exanthems, drug rash, and roseola.
395
Can children with Parvovirus B19 return to school?
Yes, once the rash appears they are no longer contagious and can return to school.
396
What are the rheumatologic manifestations of Parvovirus B19?
Arthralgia or arthritis, particularly in adolescent girls, resembling juvenile idiopathic arthritis.
397
How does Parvovirus B19 affect children with immunodeficiencies?
Can cause persistent infection leading to chronic anemia and bone marrow suppression.
398
What are the risks of blood transfusion-associated Parvovirus B19?
Although rare, transfusions may transmit the virus especially in patients requiring multiple transfusions.
399
What are the complications in children with sickle cell disease?
Transient aplastic crisis, severe anemia, fatigue, and increased risk of stroke.
400
What is the role of prenatal screening in Parvovirus B19?
Ultrasound monitoring for hydrops in at-risk pregnancies. Intrauterine transfusions may be required.
401
How can Parvovirus B19 infection be prevented?
No vaccine exists. Hand hygiene and avoiding contact with infected individuals are recommended.
402
What is the typical prognosis of Parvovirus B19 in immunocompetent children?
Excellent. Most children recover fully within 1–2 weeks without long-term complications.
403
What causes COVID-19 and how is it transmitted?
COVID-19 is caused by SARS-CoV-2, a novel coronavirus transmitted via respiratory droplets, aerosols, and fomites.
404
How does COVID-19 typically present in children?
Most children have mild symptoms or are asymptomatic. Common symptoms include fever, cough, fatigue, rhinorrhea, sore throat, and GI symptoms.
405
What are less common but significant symptoms in pediatric COVID-19?
Myalgia, anosmia, ageusia, conjunctivitis, and chest pain may be seen.
406
What is MIS-C and how is it related to COVID-19?
Multisystem Inflammatory Syndrome in Children (MIS-C) is a post-infectious hyperinflammatory condition associated with COVID-19, resembling Kawasaki disease or toxic shock.
407
What are the criteria for diagnosing MIS-C?
Persistent fever, elevated inflammatory markers, multisystem involvement, and recent SARS-CoV-2 infection or exposure.
408
What are clinical features of MIS-C?
Fever, rash, conjunctivitis, hypotension, myocardial dysfunction, abdominal pain, and elevated CRP, D-dimer, and ferritin.
409
What lab abnormalities are seen in pediatric COVID-19?
Lymphopenia, elevated CRP, LDH, D-dimer, and in MIS-C—elevated ferritin, BNP, and troponin.
410
What is the gold standard test for COVID-19 diagnosis?
RT-PCR from nasopharyngeal or oropharyngeal swab remains the diagnostic standard.
411
What role does rapid antigen testing play?
Used for screening or diagnosis when PCR is not available, though it has lower sensitivity.
412
What are the indications for hospitalization in pediatric COVID-19?
Moderate to severe respiratory distress, dehydration, shock, MIS-C, or underlying risk factors like chronic lung disease.
413
How is mild pediatric COVID-19 managed?
Supportive care at home with hydration, antipyretics, and monitoring for warning signs.
414
What is the treatment of severe pediatric COVID-19?
Oxygen, corticosteroids (e.g., dexamethasone), antivirals (remdesivir), and supportive ICU care.
415
How is MIS-C treated?
IVIG and corticosteroids are first-line. In severe cases, biologics like anakinra or tocilizumab may be needed.
416
What are cardiac complications of MIS-C?
Myocarditis, coronary artery dilatation or aneurysms, and reduced ejection fraction.
417
How is COVID-19 prevented in children?
Vaccination (depending on age eligibility), mask-wearing, hand hygiene, and ventilation.
418
What COVID-19 vaccines are approved for children?
mRNA vaccines (e.g., Pfizer-BioNTech) are approved for children ≥6 months in many countries.
419
Are children infectious carriers of COVID-19?
Yes, although they often have milder symptoms, children can transmit the virus to others.
420
What is long COVID in children?
Persistent symptoms like fatigue, brain fog, cough, or GI issues lasting weeks to months after acute infection.
421
How is COVID-19 different in neonates and infants?
Neonates may present with fever, poor feeding, respiratory distress, or be asymptomatic.
422
What is the prognosis of COVID-19 in children?
Generally excellent in healthy children. MIS-C and underlying conditions increase risk of severe outcomes.
423
What are common fungal infections in children?
Common infections include candidiasis, tinea (dermatophytosis), histoplasmosis, aspergillosis, cryptococcosis, and mucormycosis.
424
What causes oral thrush and how does it present?
Oral thrush is caused by Candida albicans. It presents as white, curd-like plaques on the buccal mucosa, tongue, and palate.
425
What are risk factors for candidiasis in children?
Antibiotic use, immunosuppression, diabetes, prematurity, prolonged hospitalization, and poor hygiene.
426
What is the treatment for oral candidiasis?
Topical nystatin or oral fluconazole in more severe cases.
427
What is diaper candidiasis and how is it treated?
Candidal diaper dermatitis presents with beefy red rash with satellite lesions. Treated with topical antifungals like clotrimazole.
428
What is systemic candidiasis and who is at risk?
Disseminated Candida infection occurs in immunocompromised children, especially those with central lines or on TPN.
429
How is systemic candidiasis diagnosed?
Blood cultures, β-D-glucan assay, and imaging for abscesses or organ involvement.
430
What are dermatophyte infections and how do they present?
Tinea infections involve skin, hair, and nails. Examples: tinea capitis (scalp), tinea corporis (body), tinea pedis (feet).
431
How is tinea capitis diagnosed and treated?
Diagnosis via KOH mount or fungal culture. Treated with oral griseofulvin or terbinafine.
432
What is histoplasmosis and where is it endemic?
Histoplasma capsulatum is endemic in river valleys (e.g., Mississippi and Ohio). Causes pulmonary or disseminated disease.
433
What are symptoms of disseminated histoplasmosis?
Fever, hepatosplenomegaly, pancytopenia, adrenal insufficiency, and respiratory symptoms.
434
How is histoplasmosis diagnosed?
Urine antigen, serum antigen, fungal cultures, and biopsy with fungal stains.
435
What is the treatment of disseminated histoplasmosis?
Amphotericin B for severe disease, followed by oral itraconazole.
436
What is aspergillosis and when should it be suspected?
Aspergillus causes invasive disease in immunocompromised children. Presents with fever, cough, hemoptysis, and chest pain.
437
How is invasive aspergillosis diagnosed?
Chest CT (halo sign), galactomannan assay, fungal culture, and histopathology.
438
What is the treatment for invasive aspergillosis?
Voriconazole is first-line. Liposomal amphotericin B is also used.
439
What is cryptococcosis and how does it present in children?
Cryptococcus neoformans causes meningitis in immunocompromised children. Presents with fever, headache, and altered sensorium.
440
How is cryptococcal meningitis diagnosed?
India ink stain of CSF, cryptococcal antigen (CrAg) test, and fungal culture.
441
What is mucormycosis and who is at risk?
An aggressive fungal infection seen in diabetics and immunocompromised. Involves sinuses, brain, lungs.
442
What is the treatment of mucormycosis?
Urgent surgical debridement plus liposomal amphotericin B. Posaconazole is used as salvage or step-down therapy.
443
What are common helminthic infections in children?
Ascariasis, hookworm infection, trichuriasis, enterobiasis (pinworm), strongyloidiasis, and schistosomiasis.
444
What is the life cycle of Ascaris lumbricoides?
Ingested eggs hatch in the intestine, larvae migrate to lungs, ascend the airway, are swallowed, and mature into adults in the intestine.
445
What are clinical features of ascariasis?
Abdominal pain, intestinal obstruction, malnutrition, and in pulmonary phase: cough, wheezing, and Loeffler syndrome.
446
How is ascariasis diagnosed?
Microscopic detection of eggs in stool. Imaging may show worms in bowel or biliary tract.
447
What is the treatment for ascariasis?
Albendazole (400 mg single dose) or mebendazole. Repeat after 2–3 weeks if needed.
448
How do hookworms affect children?
Cause iron deficiency anemia, growth retardation, and protein loss.
449
What is the pathophysiology of hookworm anemia?
Ancylostoma and Necator attach to intestinal mucosa and ingest blood, leading to chronic blood loss.
450
How is hookworm diagnosed?
Stool microscopy for eggs. CBC may show microcytic anemia.
451
What is the treatment of hookworm infection?
Albendazole or mebendazole plus iron supplementation.
452
What is enterobiasis and how does it present?
Caused by Enterobius vermicularis (pinworm); presents with perianal itching, especially at night.
453
How is enterobiasis diagnosed?
Scotch tape test in the morning detects eggs around the anus.
454
What is the treatment for enterobiasis?
Albendazole or mebendazole, repeated in 2 weeks. Treat household contacts.
455
What is trichuriasis and what symptoms does it cause?
Caused by Trichuris trichiura (whipworm); may cause abdominal pain, diarrhea, rectal prolapse, and anemia.
456
How is trichuriasis diagnosed and treated?
Stool microscopy for eggs. Treated with albendazole or mebendazole for 3 days.
457
What is strongyloidiasis and why is it important?
Caused by Strongyloides stercoralis. May cause autoinfection and disseminated disease in immunocompromised.
458
What are signs of disseminated strongyloidiasis?
Severe diarrhea, malabsorption, sepsis, meningitis, and multi-organ failure.
459
How is strongyloidiasis diagnosed?
Stool larvae detection, serology, or agar plate culture. Multiple samples may be needed.
460
What is the treatment for strongyloidiasis?
Ivermectin is the drug of choice. Albendazole is an alternative.
461
What is schistosomiasis and how is it acquired?
Caused by Schistosoma species; acquired by skin penetration of cercariae in freshwater.
462
What are complications of schistosomiasis?
Hematuria, bladder fibrosis, portal hypertension, hepatosplenomegaly, and growth retardation.
463
What is antibiotic stewardship in pediatrics?
A coordinated effort to optimize antibiotic use to improve patient outcomes, reduce resistance, and minimize side effects.
464
Why is antibiotic stewardship critical in children?
To prevent overuse, reduce adverse drug reactions, limit antibiotic resistance, and protect the pediatric microbiome.
465
What are core principles of antibiotic stewardship?
Right antibiotic, right dose, right duration, and right route.
466
Which infections often lead to unnecessary antibiotic use in children?
Viral upper respiratory infections, otitis media, bronchitis, and pharyngitis.
467
What strategies support accurate diagnosis before antibiotic use?
Thorough clinical evaluation, appropriate cultures, and use of rapid diagnostics like CRP or procalcitonin.
468
When are antibiotics indicated in acute otitis media?
In children <6 months or with severe symptoms (fever ≥39°C, otalgia >48 hrs) or bilateral disease.
469
What is the first-line antibiotic for otitis media?
Amoxicillin unless contraindicated or if resistant strains suspected.
470
When should antibiotics be avoided in pediatric diarrhea?
In non-bloody, viral gastroenteritis or non-specific diarrhea without signs of sepsis.
471
What is watchful waiting and when is it appropriate?
Delaying antibiotics to observe mild infections, often used in otitis media or sinusitis.
472
What is the recommended duration of antibiotic therapy for community-acquired pneumonia (CAP)?
Typically 5 days for uncomplicated cases, longer for severe or complicated pneumonia.
473
How does antibiotic resistance develop?
Through selection pressure that favors resistant strains, often due to inappropriate or excessive antibiotic use.
474
What are examples of narrow-spectrum antibiotics?
Penicillin, amoxicillin, and first-generation cephalosporins.
475
When are broad-spectrum antibiotics necessary?
In serious infections, polymicrobial infections, or when resistant pathogens are likely.
476
What role do antibiograms play in stewardship?
They guide empirical antibiotic selection based on local resistance patterns.
477
What is de-escalation in antibiotic therapy?
Narrowing or stopping antibiotics based on culture results or clinical improvement.
478
What are side effects of unnecessary antibiotics in children?
Diarrhea, allergic reactions, yeast infections, and long-term microbiome disruption.
479
What role does education play in stewardship?
Educating caregivers and providers improves antibiotic use and counters misconceptions.
480
What is antimicrobial cycling and is it useful in pediatrics?
Rotating antibiotic classes to reduce resistance; its role is limited and controversial in pediatric settings.
481
What are key metrics to monitor stewardship effectiveness?
Antibiotic use rates, resistance patterns, duration of therapy, and clinical outcomes.
482
How can pediatricians support stewardship daily?
Avoid empiric antibiotics without clear indications, reassess at 48–72 hours, and educate families.
