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Infection Disorder
INFECTIOUS DISORDER
| Question | Answer |
|---|---|
| Rubella (German Measles) | Rubella, or German measles, is a contagious viral infection caused by the rubella virus. It's characterized by a distinctive rash, mild fever, and flu-like symptoms. |
| Incubation of Rubella (German Measles) | Typically 14 days (range: 12–23 days). |
| Period of Communicability of Rubella (German Measles) | 7 days before to 7 days after the rash appears. |
| Mode of Transmission in Rubella (German Measles) | Spreads through direct and indirect contact with respiratory droplets. |
| Immunity for Rubella (German Measles) | Permanent after infection MMR vaccine Immune serum globulin for pregnant women exposed to rubella. |
| Signs and Symptoms in Rubella (German Measles) | Younger Children: The first sign is a pink-red maculopapular rash that starts on the face and spreads to the trunk and limbs. |
| Signs and Symptoms in OLDER CHILDREN with Signs Rubella (German Measles). | Rubella symptoms include low-grade fever, headache, malaise, anorexia, mild conjunctivitis, upper respiratory issues, swollen lymph nodes, and a 3-day rash. Some children may develop temporary arthritis. |
| Measles (Rubeola) | Definition and Causes: Measles is a highly contagious viral infection caused by the measles virus. |
| Incubation of Measles (Rubeola): | Typically 8–12 days (range: 7–18 days). |
| Period of Communicability of Rubeola | 4 days before to 4 days after the rash appears. |
| Mode of Transmission of Rubeola | Direct contact with respiratory droplets or airborne spread. |
| Immunity for Rubeola | Permanent after infection. MMR vaccine (live attenuated measles virus). Immune serum globulin |
| Signs and Symptoms of Rubeola in Prodromal Phase | (1–4 days): Three C’s (cough, coryza (runny nose), and conjunctivitis), low-grade fever. Koplik’s spots (small white spots with a bluish-white appearance on the inside of the mouth (buccal mucosa), beside the posterior molars), and occipital lymph nodes. |
| Signs and Symptoms of Rubeola in Rash Phase | Rash Phase (3–6 days): Starts behind the ears, spreads downward, with a maculopapular rash that turns brown and peels. Fever peaks at 104°F (40°C) but later subsides. |
| Management for symptomatic patient with RUBEOLA | Symptomatic treatment includes antipyretics for fever, emollients for nasal irritation, honey for cough, and light adjustments for photophobia. |
| Management for children with Measles or RUBEOLA? | Children with measles should be seen in healthcare settings after office hours to prevent exposure. Hospitalized cases require airborne precautions throughout the illness. |
| What is the vaccine to prevent individuals from getting Rubeola? | The MMR vaccine at 1 year and 4 years of age is crucial to prevent infection. |
| Smallpox (Variola) | Definition and Causes: Smallpox is a highly contagious and potentially fatal viral disease caused by the variola virus. Although globally eradicated, it remains a concern due to its potential use in bioterrorism. |
| Incubation of Smallpox (Variola) | 7 to 17 days (average 12 days). |
| Period of Communicability of VARIOLA | Contagious 24 hours before rash onset. Remains contagious until all lesions have dried, which can take up to 4 weeks. |
| Mode of Transmission in VARIOLA | Airborne transmission (highly infectious). Direct contact with an infected person. Indirect contact via objects (contaminated objects). |
| Clinical Features & Progression- Prodromal Phase of VARIOLA. | (2-4 days) High fever (101-104°F or 38.3-40°C), severe headache, back pain, and backache above the pelvis, and prostration (this phase is NOT seen in chickenpox). |
| Clinical Features & Progression-Rash Phase of VARIOLA | Within 24 hours of fever onset, flat red macules appear on the face and forearms, then spread to the distal extremities. |
| Clinical Features & Progression-Vesicular Phase of VARIOLA | Macules progress to papules, vesicles, pustules, deeply umbilicated pustules (day 7-9). Umbilicated pustules that eventually crust. |
| Rabies | Definition and Causes: Rabies is a fatal viral infection causing encephalitis, primarily transmitted through animal bites. It is caused by the rabies virus (RABV), a member of the Lyssavirus genus. |
| Incubation of Rabies | Ranges from 1 to 3 months, depending on factors like bite location and viral load. Average: 2 to 3 months. |
| Period of Communicability in RABIES | 3 to 5 days before symptom onset until death. |
| Mode of Transmission in rabies | Bites from infected animals (most common). Saliva from an infected animal enters an open wound. |
| Immunity for RABIES | Human diploid cell rabies vaccine. Rabies immune globulin (RIG). |
| Signs and Symptoms of RABIES | 🔹Prodromal: Fever, weakness, sore throat, irritability. 🔹 Neurologic: Anxiety, pain, hydrophobia, hypersalivation. 🔹 Paralytic: Paralysis → coma → death. |
| Treatment & Management for PX WITH RABIES | Once symptoms appear, rabies is nearly always fatal. Prevention is key. Post-Exposure Prophylaxis (PEP): Wash the wound with soap and water for 15 minutes. Avoid suturing unless necessary. |
| Vaccination Schedule and important notes for PX with RABIES | Day 0: Rabies vaccine + RIG (20 IU/kg) in bite area and remaining IM. Day 3, 7, 14: Additional rabies vaccine doses. RIG provides immediate antibodies, while the vaccine triggers active immunity. Start PEP if exposed to a bat, even without a bite. |
| Mumps (Epidemic Parotitis) | Definition and Causes: Mumps is a viral infection caused by the mumps virus, characterized by swelling of the parotid glands and spread through respiratory droplets. |
| Incubation of Mumps (Epidemic Parotitis) | Average: 16 to 18 days. Range: 12 to 25 days. |
| Period of Communicability of Mumps | 5 days before to 5 days after parotid gland swelling. Direct contact with respiratory droplets (sneezing, coughing, sharing drinks). |
| Immunity for MUMPS or Epidemic Parotitis | Natural immunity (lasting after infection). Active immunity: MMR vaccine (Measles, Mumps, Rubella). Immune globulin (rarely used). |
| Signs and Symptoms for MUMPS or Epidemic Parotitis | Prodromal Phase: Fever, headache, malaise, anorexia. Swelling Phase: Parotid gland enlargement (no skin redness), difficulty opening the mouth (trismus), fever. Resolution: Swelling subsides in 5–7 days. |
| Treatment & Management for MUMPS or Epidemic Parotitis | Supportive Care: (No antiviral treatment) Pain & Fever Management: Acetaminophen or NSAIDs. Soft, Bland Diet: To ease chewing. Hospitalized Patients: Droplet precautions plus standard infection control. |
| Epstein-Barr Infectious Mononucleosis | Definition and Causes: Infectious mononucleosis (IM) is caused by the Epstein-Barr virus (EBV), a member of the herpesvirus family. It is also known as glandular fever or the "kissing disease" due to its transmission through saliva. |
| Incubation of Epstein-Barr Infectious Mononucleosis | Adults & Adolescents: 30 to 50 days. Children: Shorter incubation period. |
| Period of Communicability of Epstein-Barr Infectious Mononucleosis | Direct contact with saliva from symptomatic or asymptomatic individuals. |
| Mode of Transmission of Epstein-Barr Infectious Mononucleosis | Saliva (kissing, sharing utensils, drinks). Can also spread through blood transfusions (less common) |
| Immunity for Epstein--Barr Infectious Mononucleosis | Natural immunity (lifelong). Active artificial immunity: MMR vaccine (Measles, Mumps, Rubella). Passive artificial immunity: Mumps immune globulin (rarely used). |
| Signs and Symptoms Epstein--Barr Infectious Mononucleosis | Prodromal: Anorexia, chills, fever. Acute: Fever, sore throat, lymphadenopathy, swelling. Severe: Splenomegaly, abdominal pain, atypical lymphocytes. Neurological: Meningitis, encephalitis, Guillain-Barré. |
| Diagnosis for Epstein--Barr Infectious Mononucleosis | Mononucleosis Tests: Monospot Test: Positive in 80% of children >4 years. Blood Smear: Atypical lymphocytes peak in 2–3 weeks. EBV Antibodies: IgM against viral capsid antigen (VCA) indicates primary infection. |
| Treatment & Management for Epstein-Barr infectious Mononucleosis | Pain & Fever: Use acetaminophen or NSAIDs. Rest & Hydration: Encourage cool fluids and soft foods. Avoid Contact Sports: No sports for 3 weeks to prevent splenic rupture. Recovery: Full recovery may take up to 3 months. |
| Bacterial Infections | Bacteria are single-celled organisms without a true nucleus, with their genetic material in a nucleoid. They reproduce by fission, where one cell splits into two identical cells. |
| Bacterial Shapes | Cocci (Spherical): Examples: Streptococcus, Staphylococcus. Bacilli (Rod-shaped): Examples: Escherichia coli (E. coli), Listeria. Spirillum/Spirochetes (Spiral-shaped): Examples: Treponema pallidum (syphilis), Borrelia burgdorferi (Lyme disease). |
| Classification of Bacteria Based on Staining | Gram-positive: Violet, thick wall. Ex: Streptococcus, Staphylococcus Gram-negative: Red, thin wall, extra membrane. Ex: E. coli, Salmonella Acid-fast: Waxy wall, resists acid. Ex: Mycobacterium tuberculosis |
| Scarlet Fever | Causes: β-hemolytic streptococci, group A. (The slide instructs to refer to another section for specific information on this topic). |
| Incubation Period of Scarlet Fever | Greatest during the acute phase of respiratory illness, usually 1 to 7 days. |
| Period of Communicability in Scarlet Fever | Direct contact with a person infected with scarlet fever, or large droplets, not through fomites or household pets. |
| Immunity for SCARLET FEVER | One episode of scarlet fever gives no lasting immunity to the scarlet fever toxin. No vaccination is available. |
| Additional Information for SCARLET FEVER | Scarlet fever most commonly occurs in school-age children, particularly those in the 2- to 8-year-old age group. The disease is more prevalent in temperate climates and typically occurs in late autumn, winter, and early spring (AAP, 2015). |
| Symptoms of Streptococcal Pharyngitis (Preceding Scarlet Fever): | Onset: Fever, sore throat, headache, chills, malaise, rapid pulse. Rash: Red, sandpaper-like, dense on trunk and folds (Pastia's sign). Progression: Rash desquamates after 1 week. |
| Other Symptoms of SCARLET FEVER? | Tonsils: Inflamed, enlarged, with white exudate. Palate: Pinpoint lesions, petechiae in some cases. Strawberry Tongue: White and furry (days 1-2), then red with prominent papillae (days 4-5). |
| Therapeutic Management for Scarlet Fever | Penicillin: Drug of choice for 10 days (endorsed by AHA and Pediatric Infectious Disease Society). Alternative: Amoxicillin (50 mg/kg/day) for those with penicillin G noncompliance. |
| Therapeutic Management for Scarlet Fever for Supportive Treatment: | Pain & Fever: Acetaminophen or ibuprofen. Diet: Soft or liquid foods until throat pain improves. Rash: Comfort measures. Antibiotics: Complete full course to prevent complications like acute glomerulonephritis, rheumatic fever, and reactive arthritis. |
| Diphtheria | Corynebacterium diphtheriae (Klebs-Löffler bacillus). CAUSE: Diphtheria bacilli in the nasopharynx produce a toxin causing cell death and a gray membrane. |
| Incubation Period Diphtheria | 2 to 5 days, with a range of 1 to 10 days. |
| Period of Communicability Diphtheria | In untreated persons, contagious from nares, throat, skin, and eyes for 2 to 6 weeks following infection. 48 hours after initiation of antibiotics in treated individuals. |
| Mode of Transmission Diphtheria | Direct or indirect contact with droplets. |
| Immunity for Diphtheria | Natural immunity occurs after contracting the disease. Active artificial immunity: Diphtheria toxoid given as part of the DTaP vaccine. Passive artificial immunity: Diphtheria antitoxin. |
| Assessment for patient with Diphtheria | Symptoms: Gray membrane, purulent nasal discharge, brassy cough. Complications: Myocarditis, neuritis, CNS involvement (paralysis), rare skin lesions. Diagnosis: Based on clinical signs and throat/nose cultures; lab must be notified. |
| Therapeutic Management for Diphtheria | Antitoxin: Single dose of equine antitoxin based on clinical suspicion, obtained via CDC. Antibiotics: Penicillin or erythromycin IV Management: Antitoxin and antibiotics, rest, isolation, and monitor airway obstruction. |
| Whooping Cough (Pertussis) | Bordetella pertussis. the 100-day cough, is a highly contagious, vaccine-preventable bacterial disease. |
| Incubation Period of Whooping Cough (Pertussis) | 5 to 21 days. |
| Period of Communicability of Whooping Cough (Pertussis) | Greatest during the catarrhal (respiratory illness) stage. Contagiousness persists for 5 to 7 days after starting treatment, but it can continue for weeks in untreated patients. |
| Mode of Transmission of Whooping Cough (Pertussis) | Highly contagious through direct or indirect contact with respiratory droplets. |
| Immunity for Pertussis. | Natural immunity after contracting the disease. Active artificial immunity: Pertussis vaccine as part of the DTaP vaccine. Passive artificial immunity: Pertussis immune serum globulin. |
| Assessment for Pertussis | Catarrhal Stage (1-2 weeks): Coryza, sneezing, mild cough. Paroxysmal Stage (2-6 weeks): Intense coughing fits with whooping, cyanosis, vomiting, exhaustion. Convalescent Stage (2-6 weeks): Gradual reduction in coughing and vomiting. |
| Diagnosis for Pertussis | Diagnosis: Based on symptoms; whoop sound may be absent in infants under 6 months. Diagnostic methods: PCR (early stages), culture, DFA, and serology (later stages). |
| WBC in PX WITH PERTUSSIS? | Blood Count: WBC, especially lymphocytes, can increase to 20,000–30,000/mm³ (normal is 5,000–10,000/mm³). |
| Therapeutic Management for patient with Pertussis. | Hospitalization: Infants under 3 months are hospitalized for monitoring. Antibiotics: 10-day course of erythromycin or azithromycin. Precautions: Droplet precautions for 5 days after antibiotics. |
| Complications on Pertussis | Alkalosis, dehydration from vomiting, pneumonia, atelectasis, emphysema due to plugged bronchioles. Epistaxis, subconjunctival bleeding, or seizures from asphyxia due to severe coughing paroxysms. |
| Infant Care if they have PERTUSSIS | Infants may need close monitoring for dehydration and airway management due to tenacious secretions. |
| Anthrax | Causes: Bacillus anthracis, a bacteria. |
| Incubation Period of ANTHRAX | 1 to 7 days for inhalational anthrax; 1 to 12 days for cutaneous anthrax; 1 to 7 days for gastrointestinal anthrax. |
| Anthrax's Mode of Transmission: | Originally contracted from contact with the feces of infected cows or sheep. Not transmissible from person to person. |
| Immunity for Anthrax | The anthrax vaccine is available for adults aged 18 to 65 years, particularly those who work with anthrax in labs, veterinarians handling animals or animal products contaminated with anthrax, and some military personnel. |
| Three forms of Anthrax? | Cutaneous, inhalational, and gastrointestinal. |
| Assessment for patient with Inhalational Anthrax: | Flu-like symptoms (fever, cough, fatigue), high mortality (>90%). Progresses to dyspnea, shock, and X-ray signs. Fatal if untreated, spreads via coughing, bioterrorism risk. |
| Assessment for patient with Cutaneous Anthrax: | Skin lesion starts as a papule, becomes a vesicle, and forms a painless black eschar. Symptoms: fever, malaise, headache, swollen lymph nodes. Mortality is low (1%) with treatment. |
| Assessment for patient with Gastrointestinal Anthrax: | Contracted by consuming undercooked meat contaminated with anthrax. Symptoms include severe abdominal pain, fever, bloody diarrhea, and septicemia (blood infection). The mortality rate is around 25% for this form. |
| Therapeutic Management for patient with Anthrax | Prophylaxis: Ciprofloxacin (adults) or doxycycline (children) for 60 days after exposure. Drug Therapy: First-line: Ciprofloxacin or doxycycline. Supportive care: Oxygen, fluids, and sepsis treatment for severe cases. |
| Prevention for Anthrax | Vaccination: The anthrax vaccine is not used in children, but it is available for adults such as lab workers, veterinarians, and military personnel. Prophylactic antibiotics are important for individuals at risk of exposure. |
| Tetanus | Causes: Clostridium tetani. Incubation Period: 3 days to 3 weeks. |
| Mode of Transmission of tetanus | Direct or indirect contamination of a closed wound with C. tetani spores, typically from soil or animal excretions. |
| Immunity for tetanus | Natural Immunity: Lasting immunity after disease. Active Artificial Immunity: Tetanus toxoid in DTaP vaccine. Passive Artificial Immunity: Tetanus immunoglobulin (TIG) for immediate immunity. |
| What is tetanus? | a spastic paralytic illness caused by Clostridium tetani neurotoxin. It is highly fatal if untreated, especially in individuals with deep or contaminated wounds. |
| Pathophysiology of tetanus? | Clostridium tetani spores, found in soil and animal excretions, enter the body through open wounds, producing tetanospasmin. This neurotoxin disrupts spinal cord impulses, causing muscle spasms and paralysis. |
| Symptoms of tetanus? | (lockjaw), muscle rigidity and spasms starting in the jaw and neck, respiratory distress, difficulty swallowing, opisthotonos (arched back), and autonomic disturbances like sweating, tachycardia, and fever. Severity increases with delayed treatment. |
| Diagnosis of tetanus? | Based on the history of a wound and the characteristic symptoms (lockjaw and muscle spasms). Laboratory cultures can help confirm the presence of Clostridium tetani, but clinical presentation is typically sufficient for diagnosis. |
| Therapeutic Management for Tetanus | TIG: Neutralizes toxin. Antibiotics: Eliminate bacteria. Muscle Relaxants: Control spasms. Wound Care: Clean and remove tissue. Ventilatory Support: For respiratory paralysis. Supportive Care: Manage spasms |
| Prevention to Tetanus | Immunization: DTaP vaccine in childhood, Td booster every 10 years. Post-Exposure: TIG and tetanus toxoid booster for contaminated wounds. Wound Care: Clean and manage deep or contaminated wounds properly. |
| Parasitic Infections | Parasites are organisms that live on and obtain their food supply from other organisms. |
| Pediculosis capitis | Head lice |
| Treatment for Pediculosis capitis or Head lice | Treatment: Use permethrin or pyrethrin shampoo, comb out nits. Cleaning: Wash bedding, clothes, and vacuum non-washable items. Prevention: Teach children not to share personal items like combs and hair accessories. |
| Pediculosis | Pubic lice |
| Treatment for Pediculosis or Pubic lice | Medications: Use permethrin or pyrethrin cream/shampoo. Cleaning: Wash clothes, bedding, and towels in hot water; vacuum furniture. Prevention: Avoid sharing personal items like towels or clothing. |
| Scabies | Female mite (Acarus scabiei) |
| Symptoms of Scabies? | Black burrow filled with mite feces 1–2 in. long, usually |
| Treatment for Scabies | Caution that adolescent groin infestations might be spread by physical intimacy. Topical permethrin 5% cream is the drug of choice with two doses of oral ivermectin (off-label use) 1 week apart, also being an effective drug (AAP, 2015). |
| Helminthic Infections (3) | Roundworms (Ascariasis) Pinworms (Enterobiasis) Hookworms |
| Roundworms (Ascariasis) | Information: Causes: Ascaris lumbricoides. Incubation: 8 weeks. Transmission: Ingestion of contaminated food/water with eggs. Prevention: Proper fecal disposal and hand hygiene. |
| Symptoms of Ascariasis | Often asymptomatic but can cause malnutrition, nausea, vomiting, and intestinal obstruction if the worm load is high. |
| Treatment for Ascariasis | Albendazole (single dose with food) Nitazoxanide (twice daily for 3 days) Ivermectin (off-label, not for children <15 kg) |
| Pinworms (Enterobiasis) | Information: Causes: Enterobius vermicularis. Incubation: 2 months. |
| Transmission of Pinworms | Ingesting or inhaling eggs from contaminated hands, objects, or surfaces. Auto-reinfection through scratching the anal area. |
| Prevention to Pinworms | Frequent handwashing, nail trimming. Avoid nail-biting and scratching. |
| Symptoms on Pinworms or Ascariasis | Intense anal itching, especially at night. Restless sleep, irritability, perianal redness. |
| Diagnosis on Ascariasis | Tape test (pressing transparent tape to the anus and examining for eggs). Visible worms in the perianal area. |
| Treatment for Ascariasis/ Pinworms | Mebendazole (Vermox) or Pyrantel pamoate (Pin-X) (single dose). Treat all family members. Wash clothing, bedding, towels. |
| Key Preventive Measures for Helminthic Infections | Proper sanitation and hand hygiene Washing vegetables and cooking food properly Wearing shoes to avoid hookworm infections Treating all family members in case of pinworm infection Routine deworming in endemic areas |
| Fungal Infections | Tinea Cruris (Jock Itch) Tinea Capitis (Scalp Ringworm) Tinea Pedis (Athlete's Foot) Tinea Corporis (Ringworm of the Body) |
| Tinea Cruris (Jock Itch) and its INCUBATION? | Information: Causes: Moisture, tight clothing, obesity. Incubation: 1 to 3 weeks. |
| Symptoms of Tinea Cruris (Jock Itch) | Brownish to erythematous, well-demarcated rash on the groin, inner thighs, and scrotum, possibly with papular or vesiculopapular borders. |
| Treatment for patient with JOCK ITCH | Topical antifungal for 4 to 6 weeks. Avoid corticosteroids in the area. |
| Tinea Pedis (Athlete's Foot) | Fungal infection typically caused by Trichophyton species. |
| SYMPTOMS AND TRANSMISSION OF Tinea Pedis (Athlete's Foot) | Symptoms: Itchy, red, scaly rash between the toes, burning sensation, and cracked skin. Transmission: Spread in warm, moist environments like locker rooms or public showers. |
| Treatment for Tinea Pedis (Athlete's Foot) | Topical antifungal creams (e.g., clotrimazole, terbinafine) or oral antifungals for severe cases. |
| Tinea Capitis (Scalp Ringworm) 4 TYPES | Patchy hair loss with short broken hairs (2–4 mm) b) Circular, scaly, erythematous patches with significant hair loss c) Yellow crusting d) Kerion (boggy, inflamed scalp lesion due to severe immune response) |
| Symptoms of Tinea Capitis or Scalp Ringworm | Oral antifungal (e.g., griseofulvin, terbinafine) Topical shampoo (e.g., selenium sulfide, ketoconazole) ciclopirox (2–3x per week) |
| Treatment for patient with Tinea Capitis or Ring worm | Precautions: Avoid alcohol during oral antifungal therapy (liver metabolism), avoid strong sunlight (photosensitivity) risk. |
| Tinea Corporis (Ringworm of the Body) WHAT ARE THE SYMPTOMS, Incubation, and treatment? | Symptoms: Circular, scaly, mildly erythematous lesions with central clearing and raised papular borders. Incubation: 1 to 3 weeks. Treatment: Topical antifungal for at least 1 week after lesion clears. |
| Key Preventive Measures for Fungal Infections | Keep skin dry and clean, especially in moist areas Avoid sharing personal items (combs, towels, hats, socks) Wear breathable clothing and shoes Complete full course of antifungal treatment to prevent recurrence |
| Different types of ringworm? | Ringworm of the face (Tinea faciei) Ringworm of the hand (Tinea manuum) Ringworm of the groin (Tinea cruris) Ringworm of the foot (Tinea pedis) Ringworm of the scalp (Tinea capitis) Ringworm |
| The Immune System: Structure & Function | The immune system is a network of cells, proteins, and organs that defend the body against harmful substances like bacteria, viruses, and allergens. It includes both nonspecific and specific immune responses. |
| Components of the Immune System | Physical Barriers (First Line of Defense) Nonspecific Immune Responses (Second Line of Defense) Specific Immune Response (Third Line of Defense) |
| Physical Barriers (First Line of Defense): | Skin & Mucous Membranes – Prevent entry of pathogens Cilia in Respiratory Tract – Traps and sweeps away foreign particles Normal Flora – Beneficial bacteria that inhibit pathogen growth |
| Nonspecific Immune Responses (Second Line of Defense): | Phagocytosis: White blood cells and macrophages destroy invaders. Inflammatory Response: Increases blood flow and immune activity. Complement System: Proteins that kill bacteria. Natural Killer Cells: Destroy infected and cancerous cells. |
| Specific Immune Response (Third Line of Defense) | Involves B & T Lymphocyte Creates long-term immunity through memory cells |
| Organs of the Immune System | Bone Marrow: Produces stem cells for immune cells. Thymus: Matures T cells for immunity. Liver: Produces complement proteins, contains phagocytes. Spleen, Tonsils, & Lymph Nodes: Store immune cells, filter pathogens. |
| B Cells (Humoral Immunity) – Produce Antibodies | Plasma Cells – Produce antibodies (immunoglobulins) specific to an antigen Memory Cells – Retain memory of antigen for future immunity |
| T Cells (Cell-Mediated Immunity) – Destroy Infected Cells | Helper T Cells (CD4+): Activate B cells & macrophages Cytotoxic T Cells (CD8+): Directly kill virus-infected cells Regulatory T Cells: Prevent overactive immune responses |
| IgM | Effective in agglutinating antigens as well as lysing cell walls; discovered early in the course of an infection in the bloodstream as it is the first response to pathogenic antigens. |
| IgG | he most common immunoglobulin in plasma, produced in large amounts during secondary responses. It crosses the placenta to provide infants with passive immunity, offering protection until they can produce their own immunoglobulins. |
| IgA | found in body fluids like saliva, sweat, tears, and mucus. It defends against pathogens on mucosal surfaces, especially in the gastrointestinal tract, by preventing pathogen adherence to mucosal cells. |
| IgD | Found in plasma. It may be the receptor that binds antigens to lymphocyte surfaces but its function is unclear. |
| IgE | Found in plasma. It exists bound to mast cells on tissue surfaces but mast cells are released when contacted by an antigen. It is involved in immediate hypersensitivity reactions. It is associated with allergy and parasitic infections. |
| B Cells (Humoral Immunity) – Produce Antibodies | Plasma Cells – Produce antibodies (immunoglobulins) specific to an antigen Memory Cells – Retain memory of antigen for future immunity |
| T Cells (Cell-Mediated Immunity) – Destroy Infected Cells | Helper T Cells (CD4+): Activate B cells & macrophages Cytotoxic T Cells (CD8+): Directly kill virus-infected cells Regulatory T Cells: Prevent overactive immune responses |
| HIV Infection & AIDS | HIV is a retrovirus that attacks CD4+ lymphocytes, causing progressive immunodeficiency. AIDS is the final stage of HIV infection when the immune system is severely compromised. |
| Causes & Transmission HIV Infection & AIDS | HIV-1 and HIV-2 are the two main types, with HIV-1 being the most common worldwide. The virus integrates into host DNA, leading to continuous replication and immune destruction. |
| Modes of Transmission HIV Infection & AIDS | Blood and body fluids (sexual contact, contaminated needles) Mother-to-child transmission (perinatal, breastfeeding, placenta) Blood transfusions (rare with modern screening) |
| Signs & Symptoms | Incubation: ~10 years in adults, faster in infants/children. Early Symptoms (2–6 weeks post-exposure): Fever, swollen lymph nodes, oral thrush, rash, recurrent respiratory infections, poor growth. |
| HIV Classification | (CDC Guidelines): |
| Category A (Mild) | Enlarged lymph nodes, hepatosplenomegaly, recurrent dar/sinus infections (thrush, pneumonia, herpes, CMV, toxoplasmosis) |
| Category B (Moderate) | Opportunistic infections |
| Category C (Severe/AIDS) | Severe bacterial infections, encephalopathy, PCP pneumonia, Kaposi sarcoma |
| Diagnosis for HIV/AIDS | PCR (Polymerase Chain Reaction): Detects HIV antigen in children under 18 months ELISA & Western Blot: Detect antibodies in individuals over 18 months CD4 Count: Monitors immune function (Normal: 500–1,500 cells/mm³) |
| Management & Treatment for HIV/AIDS | ART, Prevention of Opportunistic Infections: Prophylaxis for PCP pneumonia (Bactrim), Immunization: Modified vaccine schedules for HIV-positive children Prenatal Prevention: ART during pregnancy reduces mother-to-child transmission |
| HIV Infection in Pregnancy | HIV in pregnancy refers to a woman who is infected with HIV before or during pregnancy. If untreated, it can pass to the baby through the placenta, childbirth, or breastfeeding. |
| Causes & Transmission | Sexual transmission (multiple/bisexual partners, IV drug use) Mother-to-child transmission (MTCT): During pregnancy (placental transfer) During delivery (contact with infected blood) Breastfeeding |
| Signs & Symptoms Progression of HIV in Pregnancy Stage 1 (Initial Infection): | Flu-like symptoms (fever, fatigue, weight loss) |
| Stage 2 (Seroconversion (6 weeks – 1 year after exposure) | Antibodies appear in blood |
| Stage 3 (Asymptomatic Stage (3–11 years) | No obvious symptoms, but virus continues replicating |
| Stage 4 (Symptomatic HIV/AIDS (CD4 < 200 cells/mm³) | Opportunistic infections (PCP pneumonia, oral candidiasis, herpes), Kaposi sarcoma, HIV-associated dementia |
| Diagnosis for HIV/AIDS | HIV Screening Tests – ELISA & Western Blot CD4 Count & Viral Load Monitoring – Assess disease progression Routine STI Testing – Gonorrhea, syphilis, chlamydia & hepatitis B Rapid HIV Testing in Labor – If prenatal screening was missed |
| Management & Treatment for HIV/AIDS | Antiretroviral Therapy (ART) for HIV-Positive Pregnant Women Zidovudine (AZT) – Lowers risk of transmission Protease inhibitors (PI): Ritonavir, Indinavir, Saquinavir Combination Therapy: To keep CD4 > 500 cells/mm³ |
| Management & Treatment for Prevention of Mother-to-Child Transmission (MTCT) HIV/AIDS. | Cesarean birth – Reduces transmission risk Avoid breastfeeding – Formula feeding recommended Newborn Treatment: Zidovudine for first 6 weeks |
| Management of Opportunistic Infections HIV/AIDS | PCP pneumonia – TMP-SMZ (Bactrim) Kaposi sarcoma – Chemotherapy (only after the first trimester) |
| Monitoring Newborns on HIV/AID | HIV testing at birth and at 4 months If 2 negative tests by 4 months → HIV excluded |
| Allergy | An allergy is an abnormal immune system response to a typically harmless substance (allergen). It triggers an antigen-antibody reaction, causing mild to severe symptoms. |
| Causes & Triggers of Allergy | Food allergens – Milk, eggs, peanuts, shellfish Environmental allergens – Pollen, dust mites, mold, pet dander Insect stings – Bee or wasp venom Medications – Antibiotics (penicillin, sulfa drugs) Contact allergens – Latex, poison ivy |
| Diagnosis for Allergy | Skin Prick Test – Identifies specific allergens Blood Tests (IgE levels) – Measures allergic response Elimination Diet – Identifies food allergies |
| Management & Treatment for Allergy | Avoidance of Triggers – Key to preventing reactions Medications for Mild Symptoms: Antihistamines (loratadine, cetirizine) – Reduces sneezing, itching Nasal corticosteroids – Controls allergic rhinitis Topical creams – For skin rashes |
| Emergency Management (Anaphylaxis): | Epinephrine (EpiPen) – First-line treatment Seek immediate medical help Wear a medical alert bracelet |
| Allergy Shots (Immunotherapy) (Allergy) | Long-term treatment for severe allergies Helps desensitize the immune system |
| Hypersensitivity | an exaggerated immune response to an allergen, leading to tissue damage. It is classified into four types based on the immune mechanisms involved. |
| CLASSIFICATIONS OF HYPERSENSITIVITY REACTIONS: I-Immediate IgE | Involved Cell Mechanism: IgE attached to surface of mast cell; allergen triggers release of mediator. Effect: Allergies, asthma, atopic, allergic rhinitis |
| CLASSIFICATIONS OF HYPERSENSITIVITY REACTIONS: II. Cytotoxic IgG or IgM | Involved Cell Mechanism: Antigen-antibody complex precipitates; complex is activated, leading to inflammatory response. EFFECTS: Rheumatoid arthritis, systemic lupus erythematosus, serum sickness |
| CLASSIFICATIONS OF HYPERSENSITIVITY REACTIONS: IV. Delayed T lymphocyte | Involved Cell Mechanism: T cells combine with antigen; induced inflammatory reaction by direct involvement of the release of lymphokines. EFFECT: Contact dermatitis, transplant graft rejection |
| Anaphylactic Shock | Anaphylactic shock is a severe, life-threatening allergic reaction (Type I hypersensitivity) that occurs immediately after exposure to an allergen. It can cause airway obstruction, circulatory collapse, and death if not treated promptly. |
| Causes of Anaphylactic Shock | Anaphylaxis can be triggered by: Food allergens (milk, eggs, peanuts, tree nuts, shellfish) Insect stings (bees, wasps, fire ants) Medications (antibiotics, NSAIDs, anesthesia drugs) Latex exposure (gloves, balloons, medical devices) |
| Signs & Symptoms of Anaphylactic Shock | Respiratory: Wheezing, cough, SOB, throat tightness Cardiovascular: Low BP, dizziness. Skin: Hives, swelling. GI: Nausea, diarrhea. Other: Anxiety, red eyes, cramping. |
| Management & Treatment for Anaphylactic Shock EMERGENCY TREATMENT: | Administer epinephrine IM (thigh) Call 911 Position child flat with legs elevated Give oxygen if available Antihistamines (diphenhydramine) for relief Use albuterol for bronchospasm Monitor vital signs, transport to hospital for 4-6 hours |
| Long-Term Management for Anaphylactic Shock | Avoid known allergens Always carry an epinephrine auto-injector (EpiPen, Auvi-Q) Educate caregivers, teachers, and family on using an epinephrine auto-injector Wear a medical alert bracelet Consider allergist consultation for desensitization therapy |
| Drug and Food Allergies (Drug Allergies) | An unpredictable immune response to a medication, different from toxic reactions or known side effects. |
| Causes of Drug Allergies | Antibiotics (Penicillins, Cephalosporins) NSAIDs (Aspirin, Ibuprofen) Anesthesia drugs |
| Signs & Symptoms of Drug Allergies | Mild: Skin rash, urticaria (hives), itching, flushing Moderate: Swelling (angioedema), wheezing, nasal congestion Severe: Anaphylaxis (difficulty breathing, shock, loss of consciousness) |
| Management for Drug Allergies | Stop medication immediately Mild reactions: Antihistamines (Diphenhydramine) Severe reactions: Epinephrine (IM) Avoid re-exposure; wear medical alert bracelet Consult allergist for alternative medications. |
| Food Allergies | An abnormal immune response to specific food proteins (usually Type I hypersensitivity). |
| Causes of Food Allergies | Peanuts & Tree Nuts Eggs Milk Wheat Soy Seafood |
| Signs & Symptoms of Food Allergies | Immediate (within minutes to 2 hours): Hives, swelling, flushing, itching Vomiting, diarrhea, abdominal pain Wheezing, difficulty breathing; Anaphylaxis – most serious complication Delayed Reactions: Eczema flares, chronic GI issues |
| Diagnostic & Management of Food Allergy | Food Diary – Identify patterns of symptoms Elimination Diet – Remove suspected foods & reintroduce under medical supervision Skin Prick Testing & Blood Tests (IgE levels) |
| Emergency Treatment for Severe Reactions | Epinephrine (EpiPen) is the ONLY life-saving treatment for anaphylaxis Avoid ALL exposure to known allergens Wear a medical alert bracelet Educate caregivers, teachers, and family on food safety & epinephrine use |
| Stinging Insect Hypersensitivity | Common triggers: Bees, wasps, hornets, yellow jackets |
| Reaction type in Insect Hypersensitivity | Immediate Type I Hypersensitivity (Anaphylaxis) Serum sickness reactions may also occur in some cases |
| Emergency Management for Insect Hypersensitivity | First-line treatment: immediate epinephrine injection. Do NOT use antihistamines instead. Apply ice to sting site. Transport to hospital after epinephrine, as effects last 20 minutes. Kids on outdoor trips should carry an epinephrine auto-injector. |
| Long-Term Management: Immunotherapy (Hyposensitization) | Allergy shots (venom immunotherapy) reduce future reactions Contains extracts from wasp, yellow jacket, hornet, and honeybee venom Recommended after the first severe reaction |
| Prevention Tips for Hyposensitization | Avoid scented products, walking barefoot, outdoor chores, and drinking from open cans. Insects are attracted to sugar. Keep fast-acting insecticide nearby when outdoors to prevent stings. |
Created by:
Jon Anderson
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