L1: Pertussis (Whooping Cough)

Etiology & Epidemiology
  • Caused by Bordetella pertussis and occasional Bordetella parapertussis. Exclusive pathogens of humans and some primates.
  • Pathogenesis: Small, fastidious gram-negative coccobacilli. Colonizes ciliated epithelium. Expresses Pertussis Toxin (PT) which causes absolute lymphocytosis (does NOT cause the cough directly).
  • Extremely contagious (attack rate 100%). Does not survive prolonged in environment. No chronic carriers. Tetanus, Diphtheria, acellular Pertussis (Tdap) vaccine is recommended for 11-12 yr olds.
Clinical Manifestations (Stages)
  • Catarrhal Stage (1-2 weeks): Most insidious/contagious. Congestion, rhinorrhea, lacrimation.
  • Paroxysmal Stage (2-6 weeks): The hallmark. Machine-gun burst of uninterrupted cough followed by loud whoop. Posttussive emesis and exhaustion are universal.
  • Convalescent Stage (โ‰ฅ2 weeks): Symptoms gradually diminish.
  • Infants <3 months: Do not display classic stages. Present with gagging, gasping, apnea, cyanosis without classic cough/whoop.
  • Adults: No distinct stages.
Diagnosis & Treatment
  • Diagnosis: Clinical case if cough โ‰ฅ14 days with paroxysms/whoop/vomiting. Lab shows Leukocytosis (15k-100k) with absolute lymphocytosis. Note: Eosinophilia is NOT a feature.
  • Confirmation: Polymerase Chain Reaction (PCR) is test of choice from nasopharyngeal wash.
  • Treatment: Azithromycin (Drug of choice for treatment & postexposure prophylaxis). Use with caution in infants <14 days due to risk of Infantile Hypertrophic Pyloric Stenosis (IHPS). Alternative: Trimethoprim-sulfamethoxazole (TMP-SMX) for >2 months old.
  • Complications: Apnea (principal complication), pneumonia, seizures (due to hypoxia), and physical sequelae (hemorrhage, hernias). Preterm birth is significantly associated with fatal pertussis. Highest mortality in infants <6 months.
  • Prevention: Universal immunization with Diphtheria, Tetanus, acellular Pertussis (DTaP) in first 2 years + maternal immunization.

๐Ÿ’ก High-Yield Hints:

  • Suspect Pertussis if cough lasts โ‰ฅ14 days with posttussive vomiting or whoop.
  • Apnea (without cough) is the classic presentation in infants <3 months.
  • Lab hallmark is extreme leukocytosis with absolute lymphocytosis (normal small cells, NOT atypical).
  • Azithromycin is the drug of choice, but beware of IHPS (Pyloric Stenosis) in neonates.
  • Pertussis Toxin (PT) causes lymphocytosis, NOT the cough itself.

L2: Measles (Rubeola)

Etiology, Transmission & Pathogenesis
  • Highly contagious RNA virus. Humans are the only host.
  • Transmission: Airborne/respiratory droplets. Face-to-face contact not necessary (viable in air for 1 hour). Infectious 3 days before to 4-6 days after rash onset.
  • Pathogenesis: 4 phases. Causes necrosis of respiratory epithelium and small-vessel vasculitis. Infects CD4+ T cells, causing immune suppression.
Clinical Manifestations
  • Prodrome: High fever, cough, coryza, conjunctivitis. Koplik spots (pathognomonic enanthem) appear 1-4 days before rash on inner cheeks.
  • Exanthem: Maculopapular rash begins on forehead/behind ears -> spreads downward (centrifugally) to torso/extremities. Fades leaving fine desquamation.
  • Lab: Normal Erythrocyte Sedimentation Rate (ESR) and C-Reactive Protein (CRP), decreased WBCs. Diagnosis by Immunoglobulin M (IgM) detection.
Complications & Treatment
  • Pneumonia: Most common cause of death.
  • Acute otitis media: Most common complication.
  • Subacute Sclerosing Panencephalitis (SSPE): Chronic, fatal neurodegenerative complication 7-10 years later. Males > Females.
  • Treatment: Supportive. Vitamin A therapy is indicated for ALL patients to reduce morbidity/mortality (measles lowers retinol levels).
  • Prevention: Live-attenuated Measles-Mumps-Rubella (MMR) Vaccine. Contraindicated in pregnancy and immunocompromised. Postexposure prophylaxis with Vaccine or Immunoglobulin (Ig).

๐Ÿ’ก High-Yield Hints:

  • Koplik spots are pathognomonic and appear before the rash.
  • The rash spreads from the head downward (centrifugally).
  • Pneumonia = highest mortality; Otitis Media = highest frequency (complication).
  • Vitamin A must be given to ALL measles patients (prevents blindness and death).
  • SSPE is a fatal, late neurological complication occurring 7-10 years post-infection.

L3: Mumps

Etiology & Clinical Features
  • Single serotype virus. Humans only natural host. Targets salivary glands, Central Nervous System (CNS), pancreas, testes.
  • Manifestation: Bilateral or unilateral parotid swelling. Ear lobe lifted upward/outward. Pain increased by sour/acidic foods. Peeks in 3 days. Opening of Stensen duct may be red and edematous.
  • Diagnosis: Clinical + Elevated serum amylase + relative lymphocytosis. Confirmed by Polymerase Chain Reaction (PCR) or IgM.
Complications & Treatment
  • Meningoencephalitis: Most common complication. Mononuclear (lymphocytic) pleocytosis (200-600) in CSF with normal glucose.
  • Orchitis and Oophoritis: Common in postpubertal males (30-40%). Can cause testicular atrophy, but sterility is rare.
  • Pancreatitis: Fever, epigastric pain, vomiting.
  • Treatment: Supportive. Antipyretics, hydration. Vaccine: Live-virus (MMR).

๐Ÿ’ก High-Yield Hints:

  • Parotid swelling lifting the ear lobe upward and outward is classic.
  • Pain exacerbated by eating sour or acidic foods.
  • Meningoencephalitis is the most common complication (CSF shows normal glucose & high lymphocytes).
  • Orchitis is very common post-puberty, but rarely causes sterility.
  • Diagnosis is strongly supported by elevated serum amylase.

L4: Rubella (German Measles)

Acquired Rubella
  • Single-stranded RNA virus. Mild disease in children, severe in adults.
  • Clinical: Prodrome with suboccipital, postauricular, and anterior cervical lymphadenopathy. Maculopapular rash begins on face, spreads centrifugally, lasts only 3 days. Enanthem: Forchheimer spots (petechiae on soft palate).
  • Complications: Postinfectious thrombocytopenia (more in girls), Arthritis (more in adult females, involves small joints of hands).
Congenital Rubella Syndrome (CRS)
  • Most important risk factor for severe defects is the stage of gestation. Highest risk during first 8 weeks of gestation.
  • Classic Triad/Signs: Sensorineural nerve deafness (most common), Cataracts (unilateral/bilateral), and Cardiac abnormalities (Patent Ductus Arteriosus - PDA).
  • Prevention: Vaccination with live MMR vaccine. Strictly contraindicated in pregnancy. Check Immunoglobulin G (IgG) in exposed pregnant women immediately.

๐Ÿ’ก High-Yield Hints:

  • Known as "3-day measles", featuring suboccipital & postauricular lymphadenopathy.
  • Arthritis of the small joints of the hands is a common complication in adult females.
  • CRS Triad: Sensorineural Deafness (most common) + Cataracts + PDA.
  • Greatest risk of teratogenicity is infection during the first 8 weeks of pregnancy.
  • MMR Vaccine is a live vaccine and is strictly contraindicated in pregnant women.

L5: Diphtheria

Pathogenesis & Clinical
  • Caused by Corynebacterium diphtheriae (Gram-positive, aerobic, non-spore-forming bacillus).
  • Virulence: Produces a potent polypeptide exotoxin that inhibits protein synthesis causing local tissue necrosis.
  • Respiratory: Early sore throat, then formation of gray-brown leather-like adherent pseudomembrane (bleeds on removal, reveals edematous submucosa). Bull-neck appearance from massive lymph node/tissue edema. Risk of suffocation.
  • Cutaneous: Indolent non-healing ulcer with gray-brown membrane.
Complications & Management
  • Toxic Cardiomyopathy (10-25%): Responsible for 50-60% of deaths. Tachycardia out of proportion to fever, heart block, heart failure.
  • Toxic Neuropathy: Paralysis of soft palate (early), cranial neuropathies (strabismus, accommodation loss), symmetric demyelinating polyneuropathy.
  • Treatment: Equine Diphtheria Antitoxin MUST be given immediately on clinical suspicion (skin test first for hypersensitivity). PLUS antibiotics to halt toxin production: Erythromycin or Penicillin G for 14 days.
  • Prevention: Toxoid vaccines (DTaP for <7 yrs, Td for โ‰ฅ7 yrs).

๐Ÿ’ก High-Yield Hints:

  • Pseudomembrane: Gray-brown, adherent, and bleeds when scraped off.
  • Bull-neck appearance: Massive cervical lymphadenopathy and soft tissue edema.
  • Myocarditis is the leading cause of death (tachycardia out of proportion to fever).
  • Neuropathy: Paralysis of the soft palate is a very early toxin-mediated sign.
  • Give Antitoxin IMMEDIATELY based on clinical suspicion, don't wait for cultures.

L6: Parvovirus B19

Pathogenesis & Erythema Infectiosum
  • Single-stranded DNA virus. Heat and solvent resistant. Targets erythroid precursors in bone marrow causing cell lysis and transient arrest of erythropoiesis. No effect on myeloid cell line.
  • Erythema Infectiosum (Fifth Disease): Rash occurs in 3 stages: 1) Slapped-cheek facial flushing. 2) Macular erythema on trunk/extremities. 3) Central clearing gives lacy, reticulated appearance. Rash is immune-mediated (patient is NOT infectious when rash appears).
Severe Manifestations
  • Arthropathy: Frank arthritis or polyarthralgia, mostly in adult females (hands, wrists, knees, ankles).
  • Transient Aplastic Crisis: Profound sudden anemia in patients with chronic hemolytic anemias (e.g., Sickle Cell, Thalassemia). Reticulocytes drop to undetectable levels. Highly infectious during crisis (requires hospital isolation).
  • Fetal Infection: Primary maternal infection causes non-immune fetal hydrops and death (due to fetal anemia/heart failure).
  • Treatment: Supportive. Intrauterine Red Blood Cell (RBC) transfusions for hydrops. Intravenous Immunoglobulin (IVIG) for immunocompromised. No vaccine.

๐Ÿ’ก High-Yield Hints:

  • Fifth disease features the classic "Slapped-cheek" and lacy, reticulated rash.
  • In a healthy child, once the rash appears, they are no longer contagious.
  • In sickle cell patients, it causes Transient Aplastic Crisis (reticulocytes = 0).
  • Pregnant women exposed can have fetuses with non-immune hydrops fetalis.
  • Arthropathy is very common in adult females (resembles Rheumatoid Arthritis).

L7: Roseola (Exanthem Subitum / Sixth Disease)

Etiology & Clinical Features
  • Caused primarily by Human Herpesvirus 6B (HHV-6B) and occasionally HHV-7. Establishes lifelong latency in monocytes/macrophages.
  • Clinical Course: Abrupt onset of high fever (>39.7ยฐC) lasting ~3 days in an infant. As fever breaks (crisis), a faint pink or rose-colored maculopapular rash appears on the trunk.
  • Lab: Lower mean WBCs, lymphocytes, and neutrophils compared to other fevers.
  • Complication: Febrile seizures (up to 33% of patients). Encephalitis in immunocompromised.
  • Treatment: Supportive. Ganciclovir/Foscarnet/Cidofovir only for severe cases in immunocompromised.

๐Ÿ’ก High-Yield Hints:

  • Classic presentation: High fever for 3 days, rash appears exactly as fever breaks.
  • Affects infants typically around 6-9 months of age.
  • Febrile seizures are a very common presentation/complication.
  • Caused by HHV-6B which remains latent in monocytes/macrophages.
  • Unlike measles/rubella, the child usually appears well/nontoxic despite high fever.

L8: Varicella-Zoster Virus (VZV)

Varicella (Chickenpox) & Zoster (Shingles)
  • Double-stranded DNA virus. Contagious 24-48 hr before the rash is evident and until vesicles are crusted. Establishes latency in sensory dorsal root ganglia.
  • Varicella Exanthem: Intensely pruritic. Progresses from macule -> papule -> fluid-filled vesicle -> crust. Simultaneous presence of lesions in various stages of evolution is characteristic. Concentrated on trunk.
  • Herpes Zoster: Reactivation of latent virus. Unilateral, dermatomal vesicular rash. Less common in healthy children.
Complications & Management
  • Secondary Bacterial Infection: Most common (Group A Streptococcus or Staphylococcus aureus).
  • Encephalitis & Acute Cerebellar Ataxia: Gradual onset of gait disturbance/nystagmus.
  • Pneumonia: Severe complication, highly fatal in adults/immunocompromised.
  • Neonatal Varicella: High mortality if mother infected 5 days before to 2 days after delivery (no maternal antibodies passed).
  • Treatment: Acyclovir for high-risk. Prevention: Live-attenuated vaccine. Varicella-Zoster Immune Globulin (VZIG) for exposed neonates/pregnant women.

๐Ÿ’ก High-Yield Hints:

  • Rash hallmark: "Dewdrop on a rose petal" with lesions in all stages simultaneously.
  • Secondary bacterial infection (Strep/Staph) is the most common complication.
  • Cerebellar ataxia is a classic, rapid-recovery neurological complication.
  • Highest neonatal mortality if mother infected 5 days before to 2 days after delivery.
  • VZV stays latent in the sensory dorsal root ganglia and reactivates as dermatomal Zoster.

L9: Epstein-Barr Virus (EBV)

Infectious Mononucleosis
  • Double-stranded DNA gamma herpesvirus. Transmitted via saliva. Infects oral epithelial cells and B lymphocytes. Establishes latency in memory B cells.
  • Classic Triad: Fatigue, Pharyngitis (often with exudates), Generalized lymphadenopathy.
  • Other signs: Hepatosplenomegaly. Ampicillin rash (morbilliform rash if treated with beta-lactams mistakenly).
Diagnosis & Complications
  • Lab: Leukocytosis with Atypical Lymphocytes (which are antigenically activated CD8 T-cells).
  • Serology: Heterophile antibodies (agglutinate mammalian RBCs, e.g. Monospot test). For specific confirmation: IgM to Viral Capsid Antigen (VCA).
  • Complications: Splenic rupture (avoid contact sports for 2-3 weeks), Airway obstruction (treat with short-course corticosteroids). Alice in Wonderland syndrome (metamorphopsia).
  • Oncogenesis: Associated with Burkitt lymphoma (especially in malaria-endemic regions) and Hodgkin lymphoma (Reed-Sternberg cells).

๐Ÿ’ก High-Yield Hints:

  • Classic Triad: Exudative Pharyngitis, Lymphadenopathy, Fatigue.
  • Ampicillin rash: A generalized rash if incorrectly treated with Penicillins.
  • Must avoid contact sports for 2-3 weeks to prevent Splenic Rupture.
  • Atypical lymphocytes are actually antigenically activated CD8+ T-cells.
  • Oncogenic links: Burkitt lymphoma and Hodgkin lymphoma.

L10 & L11: Group A Streptococcus (GAS) & Scarlet Fever

Etiology & Pathogenesis
  • Streptococcus pyogenes (Gram-positive cocci in chains, beta-hemolytic).
  • Virulence: M protein resists phagocytosis. Immunity is type-specific to M protein.
  • Toxins: Produces Streptococcal pyrogenic exotoxins (A, C, SSA) responsible for the rash of scarlet fever.
  • Clinical: Acute pharyngitis (most common bacterial cause, 15-30%), impetigo, cellulitis.
Scarlet Fever & Diagnosis
  • GAS pharyngitis + rash caused by erythrogenic toxin.
  • Rash: Diffuse, finely papular erythema. Feels rough (goose-pimple / sandpaper rash). Blanches on pressure. Fades with desquamation.
  • Oral: Pharyngitis + Strawberry tongue.
  • Diagnosis: Rapid Antigen Detection Test (RADT) (fast) or Throat culture on sheep blood agar (Gold Standard).
Complications & Treatment
  • Suppurative: Peritonsillar abscess, retropharyngeal abscess, otitis media.
  • Non-suppurative: Acute Rheumatic Fever (RF) and Acute Poststreptococcal Glomerulonephritis (PSGN).
  • Treatment: Prevent RF by treating strictly for 10 days. Drug of choice: Oral Penicillin V or Amoxicillin. Intramuscular Benzathine Penicillin G if non-compliant. Macrolides if allergic.

๐Ÿ’ก High-Yield Hints:

  • Scarlet fever rash feels like sandpaper / goose-pimples and blanches.
  • Look for the classic Strawberry tongue + exudative pharyngitis.
  • Treating strictly for 10 days with Penicillin V prevents Rheumatic Fever, but NOT Glomerulonephritis.
  • Virulence depends on the M protein which resists phagocytosis.
  • Rapid Antigen Detection Test (RADT) is the first step; throat culture is Gold Standard.

L12: Leishmaniasis

Etiology & Pathology
  • Intracellular protozoan. Vector: Phlebotomine sandfly. Dimorphic: Promastigote in vector, Amastigote inside host macrophages.
  • Reservoir: Domestic dogs (L. infantum).
  • Visceral Leishmaniasis (Kala-azar): L. donovani (Old World), L. infantum. Causes prominent reticuloendothelial hyperplasia in liver, spleen, bone marrow. Splenic infarcts are common late in disease.
  • Immunity measured by Montenegro skin test (delayed-type hypersensitivity).
Clinical, Lab & Treatment
  • Clinical (Kala-azar): Prolonged high fever, massive hepatosplenomegaly, severe cachexia/wasting, jaundice. Highly fatal if untreated.
  • Lab: Pancytopenia (Anemia, leukopenia, thrombocytopenia) + Hypergammaglobulinemia (>5 g/dL).
  • Diagnosis: Demonstration of amastigotes in splenic/bone marrow aspirates. Serology (IgG) is very useful due to high antibodies.
  • Treatment: Pentavalent antimony (Sodium stibogluconate) for 28 days IV/IM. Liposomal Amphotericin B (highly effective 90-100% cure rate, less nephrotoxic, concentrates in RES).

๐Ÿ’ก High-Yield Hints:

  • Transmitted by the Phlebotomine sandfly; domestic dog is the reservoir.
  • Classic Kala-azar: Prolonged fever, massive splenomegaly, and cachexia.
  • Lab tetrad: Anemia, Leukopenia, Thrombocytopenia (Pancytopenia) + Hypergammaglobulinemia.
  • Pathology shows Amastigotes replicating inside macrophages (Kupffer cells/Histiocytes).
  • Liposomal Amphotericin B is highly effective (90-100%) and concentrates in the RES.

L13: Tuberculosis (TB)

Etiology & Stages
  • Mycobacterium tuberculosis (Acid-fast, obligate aerobe, lipid-rich cell wall). Airborne droplet nuclei transmission.
  • Stages: 1) Exposure. 2) TB Infection (Positive test, normal CXR, asymptomatic). 3) TB Disease (Signs/symptoms/radiographic changes).
  • Pathogenesis: Forms Primary (Ghon) Complex (parenchymal focus + regional hilar lymph node).
Clinical Manifestations & Diagnosis
  • Primary Pulmonary: Often silent. Enlarged hilar nodes can obstruct bronchi -> atelectasis.
  • Extrapulmonary: Scrofula (lymph node disease) is most common in children. Pleural effusion (WBCs with lymphocytic predominance, low glucose). Disseminated miliary TB.
  • Diagnosis: - Tuberculin Skin Test (TST): measures delayed hypersensitivity. False positives from BCG. - Interferon-gamma Release Assay (IGRA): more specific, measures IFN-ฮณ from T-cells. - Early-morning gastric acid culture (Gold Standard in young kids who swallow sputum).
Treatment & Prevention
  • Standard Regimen (6 months): 2 months of Isoniazid (INH), Rifampin, Pyrazinamide (PZA), Ethambutol, followed by 4 months INH + Rifampin.
  • Adverse Effects: - INH: Hepatotoxicity, peripheral neuropathy. - Rifampin: Orange secretions, GI upset. - PZA: Uric acid elevation. Avoid with rifampin for latent TB (fatal liver dysfunction). - Ethambutol: Optic neuritis (visual acuity/color changes).
  • Corticosteroids: Used in TB meningitis or severe miliary TB to reduce inflammation.
  • Prevention: Bacille Calmette-Guรฉrin (BCG) Vaccine (live-attenuated M. bovis). Protects against life-threatening forms in infants.

๐Ÿ’ก High-Yield Hints:

  • Ghon Complex: Local parenchymal focus + regional hilar lymph node.
  • Scrofula (Cervical lymphadenitis) is the most common extrapulmonary TB in children.
  • Early-morning gastric acid culture is the gold standard specimen for young kids.
  • Ethambutol toxicity: Optic neuritis (monitor visual acuity & color vision).
  • IGRA is more specific than TST because it doesn't cross-react with prior BCG vaccination.

L14: TORCH (Congenital Infections)

Overview & General Approach
  • Infections acquired prenatally. 1st Trimester: Malformations (heart, eyes). 3rd Trimester: Active infection (hepatosplenomegaly).
  • Jaundice: Pathologic if present at birth or within 1st 24 hours (suspect Syphilis, CMV, Rubella, Toxoplasmosis).
  • Diagnosis: Neonatal IgM has high specificity. PCR is highly sensitive/specific. Maternal IgG only indicates past exposure.
Specific Pathogens
  • Cytomegalovirus (CMV): Most common congenital infection. 90% asymptomatic at birth. Sensorineural hearing loss is the most common long-term complication. Signs: petechial rash, jaundice, microcephaly, direct hyperbilirubinemia. Diagnosis must be within first 2-3 weeks via PCR.
  • Syphilis (Treponema pallidum): Transplacental spirochete. High risk of transmission during primary/secondary maternal stages. Causes early fetal loss, prematurity, or congenital disease with protean symptoms.

๐Ÿ’ก High-Yield Hints:

  • Jaundice appearing in the first 24 hours of life is always PATHOLOGIC (think TORCH).
  • CMV is the most common congenital infection and the leading cause of sensorineural hearing loss.
  • Maternal IgG is useless for diagnosing active neonatal infection (crosses placenta); use IgM or PCR.
  • Congenital CMV requires diagnosis within the first 2-3 weeks of life.
  • Syphilis transmission is highest during maternal primary and secondary (spirochetemia) stages.

๐Ÿ“Š Comprehensive Diseases Comparison (Ultimate Cheat Sheet)

Disease Pathogen / Etiology Key Clinical Features Major Complications Treatment / Prevention
Pertussis B. pertussis (Gram -ve) Prolonged cough >14 days, whoop, posttussive emesis. Apnea in infants. High lymphocytosis. Apnea (infants), Pneumonia, Seizures, Hemorrhages. Azithromycin (beware IHPS in neonates). DTaP vaccine.
Measles (Rubeola) RNA Virus Koplik spots, downward spreading maculopapular rash, high fever. Pneumonia (most fatal), Otitis Media (most common), SSPE (late). Vitamin A (essential), Supportive. MMR Vaccine.
Mumps Single Serotype Virus Parotid swelling lifting ear lobe, pain with sour foods. Elevated amylase. Meningoencephalitis (lymphocytic), Orchitis (rarely sterile). Supportive. MMR Vaccine.
Rubella RNA Virus 3-day rash, Suboccipital lymphadenopathy, Forchheimer spots. Arthritis (adult females), Thrombocytopenia. CRS in fetus (Deafness, Cataracts, PDA). Supportive. MMR Vaccine (Contraindicated in pregnancy).
Diphtheria C. diphtheriae (Gram +ve) Bleeding gray-brown pseudomembrane, Bull-neck. Toxic cardiomyopathy (deadly), Toxic neuropathy (palate paralysis). Antitoxin (Immediate!) + Penicillin/Erythromycin. DTaP.
Erythema Infectiosum Parvovirus B19 (DNA) "Slapped-cheek", reticulated rash. Not infectious during rash phase. Transient Aplastic Crisis (Sickle cell), Hydrops fetalis, Arthropathy. Supportive. Transfusions for aplastic crisis/hydrops.
Roseola HHV-6B / HHV-7 (DNA) High fever 3 days, rash appears exactly when fever breaks (crisis). Febrile seizures. Encephalitis in immunocompromised. Supportive. (Ganciclovir/Foscarnet only if severe/immuno).
Varicella (Chickenpox) VZV (Double DNA) Intensely pruritic vesicles in ALL stages simultaneously. Secondary bacterial infection, Cerebellar ataxia, Pneumonia. Acyclovir (high risk). Live Vaccine. VZIG for exposure.
Infectious Mononucleosis EBV (DNA Herpesvirus) Fatigue, exudative pharyngitis, lymphadenopathy, atypical CD8 T-cells. Splenic rupture, Airway obstruction. Associated with lymphomas. Supportive (Avoid contact sports). Steroids for airway.
Scarlet Fever Group A Strep (GAS) Sandpaper/goose-pimple rash, Strawberry tongue, exudative pharyngitis. Rheumatic Fever (RF), Poststreptococcal Glomerulonephritis (PSGN). Penicillin V for 10 days (prevents RF).
Leishmaniasis Protozoan (Sandfly) Massive splenomegaly, cachexia, pancytopenia, hypergammaglobulinemia. Secondary bacterial infections, Bleeding. Highly fatal if untreated. Liposomal Amphotericin B or Pentavalent antimony.
Tuberculosis (TB) M. tuberculosis Ghon complex, Scrofula (nodes), Cavitary lung lesions. Miliary TB, TB meningitis, Obstruction/atelectasis. 6-mo regimen: INH, Rifampin, PZA, Ethambutol. BCG Vaccine.
Congenital CMV Cytomegalovirus Pathologic Jaundice (<24hr), petechiae, microcephaly. Sensorineural hearing loss (most common long-term), MR. PCR within first 2-3 weeks. Antivirals (Ganciclovir).