This document provides information on various types of hepatitis, including Hepatitis A, B, C, D, E, and G. It discusses modes of transmission, symptoms, treatments, and prevention strategies for each. Key points include:
- Hepatitis A and E usually cause self-limited illness, while Hepatitis B, C, and D can lead to chronic infections and liver damage.
- Hepatitis B can be transmitted sexually or from mother to baby and has a vaccine, while Hepatitis C is usually transmitted through blood and currently has no vaccine.
- Prevention strategies for Hepatitis A include handwashing, food handling hygiene, and vaccination, while Hepatitis B prevention focuses on vaccination, safe medical practices
This document provides information on various types of hepatitis, including Hepatitis A, B, C, D, E, and G. It discusses modes of transmission, symptoms, treatments, and prevention strategies for each. Key points include:
- Hepatitis A and E usually cause self-limited illness, while Hepatitis B, C, and D can lead to chronic infections and liver damage.
- Hepatitis B can be transmitted sexually or from mother to baby and has a vaccine, while Hepatitis C is usually transmitted through blood and currently has no vaccine.
- Prevention strategies for Hepatitis A include handwashing, food handling hygiene, and vaccination, while Hepatitis B prevention focuses on vaccination, safe medical practices
This document provides information on various types of hepatitis, including Hepatitis A, B, C, D, E, and G. It discusses modes of transmission, symptoms, treatments, and prevention strategies for each. Key points include:
- Hepatitis A and E usually cause self-limited illness, while Hepatitis B, C, and D can lead to chronic infections and liver damage.
- Hepatitis B can be transmitted sexually or from mother to baby and has a vaccine, while Hepatitis C is usually transmitted through blood and currently has no vaccine.
- Prevention strategies for Hepatitis A include handwashing, food handling hygiene, and vaccination, while Hepatitis B prevention focuses on vaccination, safe medical practices
Pediatrics: Oral and Written Revalida > Percutaneous HbIg + vaccine (0.
6 mg/kg within 24 hours)
Hepatitis > Vaccination: Deep IM (deltoid or anterolateral part of thigh) Inflammation of the liver > Treatment: None Usually affect older children Infectious Hepatitis C Viruses (TORCH) hypertropic viruses goes straight to the liver and Incubation = 7- 9 weeks causes Hepa A,B, C,D, E, F Chronicity = 85% increased risk of liver failure/ cancer Bacterial – typhoid, TB, gram (-) E.coli Risk factors: Parasitic a. Blood pressure = most important Non-Infectious b. Sexual Drugs (anti-TB drugs) c. Perinatal transmission Chemicals (anesthetics) d. Hemodialysis Viral Hepatitis e. IV drug abusers Physical Findings: No treatment or vaccine Jaundice 90% Hepatic tenderness 85% Hepatoma 70% Splenomegaly 20% Hepatitis D Spider angiomata +/- Smallest Treatment: Delta agent, defective RNA virus Supportive Replicates only when associated with Hepa B, exists as either Regular diet coinfection or superinfection - If patient has abdominal pain & intolerance to Incubation: 2-8 weeks fat → decrease fat intake Chronic Hepa D may lead to cirrhosis or even death Hepa A and E are not known to cause chronic illness, whereas Hepa B, C, D Management is generally supportive can cause significant morbidity and mortality through chronic infections Hepatitis E Enterically transmitted, similar course to Hepa A Hepatitis A Non A and Non B Maybe aymptomatic, mild non-specific in children (anicteric 15-34 y/o hepatitis) HEV IgM/IgG Fecal-oral transmission No treatment, no vaccination Incubation period = 4 weeks Hepatitis G 0-4 weeks = body weakness, anorexia, fever HGV RNA 4th week = fecal shedding (very infectious shedding) 10-20% adult with HBV/HCV/HDV Serology = anti-HAV BloodBorne - IgM-presence means acute Hepa A Organ transplantation - Prognosis=complete recovery Persistent viremia with normal ALT 1. Hygiene/Sanitation No histologic insult a. food handling It is not clear if HGV is a pathogen b. hand washing c. enteric presentation Differential Diagnosis: 2. Vaccination The probable causes of hepatitis vary by age. In the newborn a. post exposure prophylaxis within 2 weeks (among period, infection remains an important cause of hyperbilirubinemia households) but metabolic and anatomic causes (biliary atresia, choledochal - Ig cyst) also must be considered. - HAV vaccine In later infancy and childhood: - hemolytic-uremic syndrome Hepatitis B - Reye and Reye-like syndrome One of the forerunners of hepatocellular carcinoma - Malaria, leptospirosis, brucellosis and with severe Transmission: infection Fecal –oral route In older children , adolescents Percutaneous – blood borne - Gallstones Sexual - Chronic hemolytic process Vertical – mother to baby - Wilson’s disease, cystic fibrosis, systemic lupus HbeAg + Mom = 70-90% infant carrier erythematosus Incubation period: 45-160 Medications, including acetaminophen overdose, valproic acid, Hepa B course: Vertical Transmission various hepatotoxins such as long-acting mushroom toxins Hepa B Virion (+) anti-Hbe= px not replicating anymore (+) HbeAg = very infectious IgM- recent (active) IgG = post Prevention (no treatment) Prenatal screen for hepa B Blood donor screen Enteric precautions (stool disposal) Safe sex Nursery: wear gloves Rinse off amniotic fluid Immunization (most important) Plasma/ yeast derived
Hepatitis B Post-Exposure Prophylaxis
- perinatal > HbIg + vaccine within 24 hours (give Ab 1st before Ag Pneumonia Radiographic appearance alone not diagnostic other clinical is an inflammation of the parenchyma of the lungs features must be considered caused by: microorganisms (most cases) The peripheral WBC count useful in differentiating viral from noninfectious causes include: bacterial pneumonia: - aspiration of food or gastric acid, foreign bodies, > Viral: WBC normal or elevated but not 20,000/mm3 with a hydrocarbons, & lipoid substances lymphocyte predominance - hypersensitivity reactions >Bacterial: elevated WBC count 15,000-40,000/mm3 and - drug or radiation induced pneumonitis predominance of granulocyte classified on an anatomic basis: lobar or lobular, alveolar, or Definitive diagnosis: isolation of a virus from respiratory tract interstitial process secretions Specific risk factors: Growth of a respiratory virus in tissue culture usually takes 5-10 Lung disease-asthma/ cystic fibrosis days Anatomic problems – tracheoesophageal fistula Reliable reagents for the rapid detection of RSV, parainfluenzae, GERD w/ aspiration influenzae, and adenoviruses are available Neurologic disorders that interfere with protection of the airway Serologic techniques or compromise clearing of the airway can be used to diagnose a recent respiratory viral infection Diseases that alter the immune system – immunodeficiency laborious, slow, and not generally clinically useful, as the infection diseases or hemoglobinopathies usually is resolved by the time it is confirmed serologically. Most common cause: respiratory syncytial virus (RSV) Serology useful as epidemiologic tool to define the incidence and > especially children <3 y/o prevalence of the various respiratory viral pathogens Other causes: parainfluenza, influenza, and adenoviruses Treatment: Pathophysiology: Amoxicillin – mildly ill children who do not require The lower respiratory tract is normally kept sterile by physiologic hospitalization defense mechanisms, including the mucociliary escalator, the High doses of amoxicillin (80-90 mg/kg/24hr) in communities properties of normal secretions such as secretory IgA and clearing with high % of penicillin-resistant pneumococci of the airway by coughing. Therapeutic alternatives: Immunologic defense mechanisms of the lung that limit invasion cefuroxime axetil or amoxicillin/clavulanate by pathogenic organisms include macrophages that are present in azithromycin (school-aged children with suggestive M. alveoli and bronchioles, secretory IgA, and other immnoglobulins. pneumoniae infection) Viral pneumonia results from spread of infection along the airways, accompanied by direct injury of the respiratory epithelium Hospitalized children: resulting in airway obstruction from swelling, abnormal secretions, Bacterial: Parenteral cefuroxime (75-150mg/kg/24hr) and cellular debris. Staphylococcal pneumonia: include vancomycin/clindamycin Bacteria typically enter the lung when airborne droplets are inhaled, but they can also reach the lung through the bloodstream If viral pneumonia: withhold antibiotic therapy when there is an infection in another part of the body. Many Reserved for patients who are mildly ill bacteria live in parts of the upper respiratory tract, such as the (+) clinical evidence of viral infection nose, mouth and sinuses, and can easily be inhaled into the alveoli. (-) respiratory distress Once inside the alveoli, bacteria may invade the spaces between cells and between alveoli through connecting pores. This invasion Complications triggers the immune system to send neutrophils, which are a type Result of direct spread of bacterial infection within the thoracic of defensive white blood cell, to the lungs. The neutrophils engulf cavity and kill the offending organisms, and they also release cytokines, pleural effusion causing a general activation of the immune system. This leads to emphysema the fever, chills, and fatigue common in bacterial and fungal pericarditis pneumonia. The neutrophils, bacteria, and fluid from surrounding bacteremia & hematologic spread blood vessels fill the alveoli and interrupt normal oxygen rare complications: meningitis, suppurative arthritis, osteomyelitis transportation. Bacteria often travel from an infected lung into the bloodstream, causing serious or even fatal illness such as septic shock, with low blood pressure and damage to multiple parts of the body including the brain, kidneys, and heart. Bacteria can also travel to the area between the lungs and the chest wall (the pleural cavity) causing a complication called an empyema. Clinical Manifestations Viral & bacterial pneumonia: preceded by several days of respiratory symptoms-rhinitis and cough Often other family members are ill Viral pneumonia: (+) fever but temperatures are generally lower than in bacterial pneumonia Most consistent clinical manifestation of pneumonia: Tachypnea Increased work of breathing accompanied by: intercostals, subcostal, & suprasternal retractions nasal flaring use of accessory muscles Severe infection may be accompanied by: cyanosis & respiratory fatigue especially in infants . Auscultation: crackles & wheezing, often difficult to localize source in very young children with hyperresonant chest Difficult to clinically differentiate viral pneumonia from disease by Mycoplasma and other bacterial pathogens Diagnosis: Chest radiograph confirmatory may also indicate complication such as pleural effusion/ emphysema Viral pneumonia: hyperinflation with bilateral interstitial infiltrates & peribronchial cuffing Pneumococcal pneumonia: confluent lobar consolidation Dengue Fever From 2nd-6th days of fever, nausea & vomiting are apt to occur, & – a benign syndrome caused by several arthropod-borne viruses generalized lymphadenopathy, cutaneous hyperesthesia or – characterized by biphasic fever, myalgia or arthralgia, rash, hyperalgesia, taste aberrations, & anorexia. leucopenia, & lymphadenopathy About 1-2 days after defervescence → a generalized, morbilliform, Dengue hemorrhagic fever maculopapular rash appears (spares the palms & soles). It - is a severe, often fatal, febrile disease caused by dengue viruses disappears in 1-5 days; desquamation may occur - characterized by capillary permeability, abnormalities of Rarely there is edema of the palms & soles hemostasis, & in severe cases, a protein losing shock syndrome About this time, second rash appears, the body temperature may (Dengue shock syndrome). become slightly elevated & demonstrate the characteristic Etiology: BIPHASIC temperature pattern. Aedes aegypti – a daytime biting mosquito is the principal vector; Dengue Fever breeds in clean water, rainwater collected in container - Acute febrile illness with no identifiable focus of infection of 2-7 days Dengue hemorrhagic Fever duration with 2 or more of the following. - endemic in tropical areas of America and asia. Headache - Can occur during the primary dengue infections, mostly infants Retroorbital pain whose mothers are immune to dengue. Myalgia - Second dengue infections are mild in majority of instances Arthralgia Replication and Transmission of Dengue Virus 1. Virus transmitted to human in mosquito Rash Saliva Hemorrhagic manifestation (petechiae + tourniquet test) 2. Virus replicates in target organs Lecopenia 3. Virus infects white blood cells and lymphatic tissues Dengue Hemorrhagic Fever 4. Virus released and circulates in blood The following must all be present: 5. Second mosquito ingests virus with blood Fever, or hx of acute fever, lasting 2-7 days 6. Virus replicates in mosquito midgut Hemorrhagic manifestation include: and other organs, infects salivary glands - positive tourniquet test 7. Virus replicates in salivary glands - petecchiae, eccyhmoses or purpuric rashes Hypothesis on pathogenesis of DHF: - bleeding like epistaxis, gum bleeding, hematemesis, Persons who have experienced a dengue infection develop serum melena antibodies that can neutralize the dengue virus of that same Thrombocytopenia (< 100,000 cells per mm3 or less) or 1-2 (homologous) serotype platelets/oil immersion field In a subsequent infection, the pre-existing heterologous antibodies Evidence of plasma leakage due to increased vascular permeability form complexes with the new infecting virus serotype, but do not manifested by at any or more of the following: neutralize the new virus Hematocrit > 40% or a raise of > 20% in hematocrit for age & sex Antibody-dependent enhancement is the process in which certain A drop in > 20 % hematocrit following volume replacement strains of dengue virus, complexed with non-neutralizing treatment as compared to baseline antibodies, can enter a greater proportion of cells of the Signs of plasma leakage & hypoproteinemia mononuclear lineage, thus increasing virus production. Infected monocytes release vasoactive mediators, resulting in Dengue Shock Syndrome increased vascular permeability and hemorrhagic manifestations All of the above criteria for DHF must be present, plus evidence of circulatory that characterize DHF and DSS failure manifested by: Pathogenesis: Rapid and weak pulse Acute illness and viremia 3-7 days Narrow pulse pressure (< 20 mmHg) or manifested by: Recovery or progression to leakage phase Hypotension for age (< 80mmHg systolic pressure for < 5 years of Dengue virus enters and replicates within monocytes, mast cells, age and < 90mmHg systolic pressure for > or = 5 years of age) and fibroblasts Cold, clammy skin and restlessness Innate and adaptive immune response Grading Severity of DHF: Cytokine release: TNF-a, IL-2, IL-6, IL-8 Grade 1 Compliment activation Fever and nonspecific constitutional symptoms Antibody dependent enhancement (ADE) thought to contribute to Positive tourniquet test is only hemorrhagic severe infections manifestation T-cell activation: CD4 and CD8 cells cytokine production Grade 2 Capillary Leak Syndrome: manifestations + spontaneous bleeding (skin or • Transient increased capillary permeability due to endothelial cell other hemorrhages dysfunction Grade 3: • Widening of tight junctions Signs of circulatory failure (rapid/weak pulse, • Cytokine release and complement activation narrow pulse pressure, hypotension, Leukopenia, Thrombocytopenia and Hemorrhagic diathesis: cold/clammy skin) • Direct viral bone marrow suppression Grade 4 • Platelet destruction in DHF Profound shock (undetectable pulse and BP) • Molecular mimicry between viral protein and coagulation factors The only difference between DF and DHF grade I is the presence Clinical Manifestations: of thrombocytopenia and hemoconcentration Incubation period: 1-7 days Criteria and indication for admission: Variable & are influenced by age of the px Danger Signs: In Infants & young children: Fever of 1-5 days, pharyngeal - spontaneous bleeding inflammation, rhinitis, & mild cough. - persistent abdominal pain Infected older children & adults: sudden onset of fever, w/ - persistent vomiting temperature rapidly increasing to 39.4-41.1 C. accompanied by - changes in mental status frontal or retro-orbital pain. Occasionally severe back pain - restlessness precedes the fever (back-break fever). - weak and rapid pulse A transient, macular, generalized rash that blanches under pressure - cold, clammy skin – seen during the 1st 24-48 hr of fever. - circumoral cyanosis Pulse rate- slow relative to degree of fever - difficulty of breathing Myalgia & arthralgia –occur soon after onset & increase in - seizures severity. - hypotension or narrowing of pulse pressure (<20 mmHg) - platelet count < 100,000 cells per mm3 - hemoconcentration - prolonged bleeding time (> 5 minutes by Ivy method) Laboratory criteria for confirmation of DF are: Serological Confirmation: Demonstration of a fourfold or greater change in IgG antibody titers to one or more dengue virus antigens in paired serum samples Anti-Dengue IgM Elisa positive Sample for serological confirmation 1. 3-5 sample, (refrigerated & sterile) obtained during acute and convalescent phase 2. complete clinical information Virological Confirmation - Isolation of the Dengue virus from serum or autopsy samples - Demonstration of the dengue virus antigen in all serotypes by immunoflourescence or immunoperoxidase test -Demonstration of dengue virus genome by RT-PCR using dengue consensus and serotypes specific primers
Differential Diagnosis
Viral: Influenza, HIV, Hepatitis A, Yellow Fever, Hantavirus, Measles,
Rubella, Coxsackie and other enteroviruses, parvovirus B19, Chikungunya virus, EBV Bacterial: Typhoid, Scarlet fever, Meningococcemia Parasitic: Malaria, Leptospirosis, Rickettsial disease, Leishmaniasis, Chagas disease Fungal: Cryptococcus, Blastomycosis, Histoplasmosis Non-Infectious: Malignancy, rheumatic, vasculitis, drug fever, other miscellaneous
Mosquito Borne Illnesses
Protozoa: Malaria Roundworm: Filariasis, dirofilariasis Alphaviruses: Chikungunya fever, Mayaro fever, Ross River fever, Eastern, Western, and Venezuelan equine encephalitis Flaviviruses: West Nile fever, Zika fever, St. Louis encephalitis, Japanese encephalitis, Yellow Fever Bunyaviruses: LaCrosse encephalitis, Oropouche virus, Bwamba fever, California encephalitis
Treatment:
Treatment of uncomplicated dengue fever is supportive. Bedrest is
advised during the febrile period. Antipyretics should be used to keep body temperature less than 40 C (104 F). Analgesics or mild sedation may be required to control pain. Aspirin is contraindicated and should not be used because of its effects on hemostasis. Fluid and electrolyte replacement is required for deficits caused by sweating, fasting, thirsting, vomiting, and diarrhea.