Infectious and Communicable Diseases PDF

Infectious and Communicable Diseases Definition of Terms: Based on the setting: Disease – causes a detectable alteration in the normal a. HAIs – hospital-associated infection. Types: tissue function of the human body; ma...

Infectious and Communicable Diseases Definition of Terms: Based on the setting: Disease – causes a detectable alteration in the normal a. HAIs – hospital-associated infection. Types: tissue function of the human body; manifested and Nosocomial – developed d/t client’s stay in the presented by signs and symptoms. facility; not related to client’s diagnosis and not o Non-communicable disease – focus on the internal present during time of admission. Appears 48-72 changes in the human body hrs after admission and can occur after discharge o Communicable disease – contagious; also considers Iatrogenic – procedure or treatment related the external environment (microorganism life) of infection (ex: surgical site infection, catheter- the human body. Primarily the cause of mortality related infection) gap between the rich and poor. Factors include: b. CAIs - community-acquired infection – due to local ▪ Infectious agents transmissions ▪ Transmission Infection – successful implantation, inoculation, Based on source of infection: replication of a microorganism in an organ or tissue Endogenous – caused by overgrowth of organisms where it is not normally found (microbial flora) that are normally present in the body Contagion – with exposure or contact from an infected that were previously inapparent or dormant (ex: person which stimulates the transmission of the disease bacterial vaginosis) Infectious disease – infection that leads to a disease Exogenous – pathogen enters the body from an external with manifested signs and symptoms; disease caused by source invasion and multiplication of microorganisms Opportunistic infection – pathogen has the Contagious disease – exposure or contact causes signs “opportunity” to cause disease d/t and symptoms of a disease. Ex: STDs, respiratory immunocompromised status or poor defense system of diseases the patient. Pathogen does not cause disease in a Virulence – refers to the power or strength of the normal, healthy individual. organism to cause a disease as seen in manifestations NOT all infections or contagions can lead to a disease. Epidemiology NOT all infectious diseases are contagious study of patterns and occurrences of the disease and ALL contagious diseases are infection diseases. the backbone for disease prevention and control. Study of distribution (time, places, people) and HIV – previously called simian infection virus (SIV) from determinants (holistic factors that affect health) of exposure to infected monkey blood which mutated into the health-related events in specific populations human immunodeficiency virus (HIV) Used in the assessment of a community or evaluation of interventions in community health practice (ex: IMCI) Stages of a Disease: Spanish flu – occurrence helped establish the protocols 1. Incubation period – from first exposure to causative for highly infectious diseases agent to the appearance of initial symptom. Smallpox – totally eradicated worldwide since there is no Duration of incubation period does not reflect the animal involvement; only person-person transmission fatality of the disease due to presence of dormant Patterns of Disease: stage (ex: HIV – 5-10 yrs, rhabdovirus – up to 20 yrs) a. Endemic – constant, continuous, consistently present in Shorter incubation period reflects higher virulence of a population or community (ex: dengue, tuberculosis, the pathogen. malaria, leptospirosis). Immunity is developed. Longer incubation period means the disease is more b. Epidemic – sudden increase in the # of cases – outbreak communicable due to increased exposure with other of disease in a relatively short period of time. Can lead people who are not infected. to a pandemic crisis (ex: polio outbreak, SARS outbreak, 2. Prodromal period – AKA catarrhal period which begins MERS-COV). Person to person epidemics involve a with the appearance of initial symptoms to the gradual build-up of cases. appearance of classical/pathognomonic signs of the c. Sporadic – on and off occurrence of the disease (ex: disease. With early and mild symptoms tetanus, botulism, rabies) Pathognomonic – specific to a disease d. Pandemic – epidemic disease that spreads worldwide. If Classic sign – common sign of the disease but not it happens, the goal is to make it endemic. definitive/confirmatory Indicators of Epidemiology: 3. Stage of Illness – overt signs and symptoms: all 1. Morbidity – prevalence and incidence manifestations are out; “full blown” infection 2. Mortality – considers vital statistics 4. Convalescent stage – stage of recovery and return to 3. Health indicators – quantitative measures (rates and pre-diseased state ratios) that describe and summarize health status of the population; also includes determination that contribute Types of Infection: to causation and control of disease Based on affected body systems: Local infection – regional transmission in the body only Epidemiologic Triad Systemic infection – spread to other organs of the body 1. Agent – organism involved in the disease Based on severity or duration of disease: a. Infectivity – ability of the agent to enter the Acute infection – fast and sudden appearance of s/sx human body (external) and move into tissues and lasts for a short period of time; usually self-limiting (internal) Chronic infection – slow progression of the disease. not b. Virulence – strength, potency, or power of a all chronic infection come from acute stage (dormant causative agent to cause disease or manifest stage of the disease) systems  c. Antigenicity – ability of an agent to trigger Parasite Organisms that live off Internal – tapeworm, antibody response. All microbes carry antigen and consume the roundworms, hook but not all microbes can trigger antibody resources of the host worms, liver fluke response External - lice, ticks, d. Pathogenicity – ability to cause a disease mites, fleas, scabies 2. Host – organism that harbors and provides nutrition for Ascariasis, the agent. Multiple factors influence ability of the host enterobiasis to fight agents (age, gender, socioeconomic status, Fungi least common to cause Ringworm, tinea nutrition, immunity) disease since it is almost capitis, tinea pedis, 3. Environment – condition in which the agent may exist, present everywhere tinea cruris survive, or originate. a. Physical – temperature, weather, soil, water Reservoir b. Biological – animals, insects, flora Any person, animal, substance in which a causative c. Socioeconomic – behaviors, personality, agent normally lives and multiplies and depends attitudes, culture, urbanization primarily on survival and reproduces in numbers so that it can be transmitted to a susceptible host Chain of Infection Portal of Exit The way pathogens get out of the reservoir Usually carried through body fluids (e.g., blood, secretions) from the GI, respiratory, genitourinary, skin, and mucous membranes. Mode of Transmission Mechanism by which a pathogen is spread from reservoir to susceptible host Weakest link in the chain: agent travels and is affected by environmental conditions Defines the level of communicability of disease Contact transmission – most frequent mode of transmission Types: 1. Direct Contact - person to person transmission by physical contact without any intermediate object Causative Agents/Pathogens: involved. Can be done through sexual contact, touching, The biologic agent that is capable of causing the disease kissing. Also refers to contact with infected soil or Rule: know the agent to give the proper treatment to vegetation the disease. This can be done through culture and a. Droplet spread – transmits within 3 ft spray; sensitivity (C&S) with relatively large, short-range aerosols All organisms have the goal to survive – mutation can through sneezing, coughing, or talking. (ex: happen to maintain existence pertussis, meningococcal infection) 2. Indirect transmission – reservoir transfers through air Viruses self-limiting, Dengue virus, suspension, inanimate objects, and animate intracellular organisms measles, viral intermediaries which requires host cells hepatitis, herpes, a. Airborne – transmits beyond 3 ft; agent is in order to propagate influenza, meningitis carried by dust, vapor, or small particle Bacteria o most common TB, pneumonia, aerosols (droplet nuclei) suspended in air for infectious agent that typhoid fever. long periods of time (ex: measles, causes fatal diseases Chlamydia tuberculosis). worldwide trachomatis, Viveo b. Aerosol – with a pressure/force that enables o bacteria carry toxins if cholerae, botulism, C. the particle to be suspended for a longer they are spore- difficile, B. anthracis. periods of time forming which are Clostridium tetani are c. Vehicle – food, biologic products, drugs, deadly. spore-forming fomites (ex: HIV, hepatitis virus, C. botulinum) o Cocci – round shaped bacteria which have d. Vector – insects such as mosquitoes, fleas, o Bacilli – rod shaped protective layers that ticks carry agent through mechanical means o Spirilla – twisted contain has a toxin and support their growth (ex: shigella, malaria, shape (ex: tetanospasmin) dengue) Protozoa larger than bacteria; Plasmodium species Portal of Entry smallest single-cell with falciparum as the Path by which agent enters the susceptible host. Path is organisms which are most dangerous since usually the same with the portal of exit but usually capable of sexual it has the ability to refers to holes or cavities in the body (mouth, vagina, propagation enter the meninges anus, eyes, wound) and brain (meningoencephalitis) Susceptible Host Amebiasis, giardiasis Individual that lacks barriers or effective resistance to the invasion and multiplication of agents  Supporting defenses of host considers age, hygiene, 4. Isolation – measures to prevent spread of infection to nutrition, fluids, sleep, stress, and immunizations. healthy clients by separation of infected clients a. Category-specific – strict, contact, respiratory, Lines of Defense: enteric, drainage, blood, and body fluids 1. Primary – skin and mucous membranes b. Disease-specific – for a specific disease; use of 2. Secondary – inflammatory response: cytokines, rooms with special ventilation or cohorting for histamine, prostaglandins patients with the same disease 3. Tertiary – immune response. Immunology – study of the immune system in Infection Prevention and Control relation to diseases. Standard or Universal Precautions – to be used in all hospitalized Immunity – “immunis”; to be exempted. clients regardless of diagnosis or infection status. Used in handling Immunization – involves introduction or of blood and body fluids, non-intact skin, and mucous administration of external agents that will membranes. Includes: trigger immune response a. Hand hygiene – the most effective way to prevent Antibody – y-shaped proteins that attach to infection. Considerations: the antigens on the surface of the pathogen to Use at least 4mL of hand soap with running water. weaken the cellular membrane Friction should be present and should last at least 20 secs. Two types of immune response: 5 moments: before touching px, before performing a 1. Innate immune response – present since birth (physical procedure, after exposure to any fluids, after touching a defenses, normal flora, cilia, acidic environment of GI) px, after touching the surroundings 2. Adaptive immune response a. Humoral (Antibody-mediated) – antibodies weaken, b. Personal protective equipment destroy, or denature the structure of pathogens; Donning of PPE Doffing of PPE triggered by presence of detectable antigens. GOWMA-GogGlov GlovGog-GOWMA Memory cells allow faster response for second Clean gloves should be used in handling body fluids exposure to the same antigen. and contaminated items. Perform hand hygiene b. Cellular (Cell-mediated) – T-cells support lysis and before and after use phagocytosis of pathogens (lymphocytes, Masks, goggles, and face shields are used when macrophages, CD4 cells, lymphokines) there is a risk for splashes or sprays of contaminated fluids. Methods of Breaking the Chain of Infection: Gown is intended to protect clothing from splashes. 1. Hand hygiene – most effective prevention infection measure. Must be done regularly before and after c. Safe injection practices providing care Place needles directly in sharps container: white, a. Clean technique – keep hands below the translucent, or opaque, puncture and spill proof. elbows. Used for clean procedures to reduce Empty container when ¾ full. and prevent spread of infection Dispose needles immediately after use. b. Surgical technique – keep hands above Standard: triple gloving. Minimum: double gloving elbows. Used in surgical and invasive Do not recap needles or use two-hand technique. procedures, wound care to eliminate all Use one-hand scoop technique. microorganisms Do not bend or carry syringes in your pocket. 2. Disinfection – use of antiseptics and disinfectants which First Aid for needlestick injuries: have bactericidal (destroy bacteria) and bacteriostatic o Let the wound bleed under running water. (prevent growth) properties Wash the wound with soap and running a. Antiseptic – used on skin or tissues water. Do not suck the wound. b. Disinfectants – more concentrated and used o Flush or irrigate the eyes using clean, NSS, or on inanimate objects or surfaces; can be toxic sterile water if. to human tissue o Report incident to the supervisor. 3. Sterilization – destroys all microorganisms including o Treat with post-exposure prophylaxis. spores and viruses. Methods include: a. Moist heat – through autoclave; steam under d. Safe handling and disposal of contaminated objects pressure attains temperature higher than Handle soiled items carefully and as little as possible. boiling point (121 C) for at least 30 mins Do not shake it. Bundle it up with clean side out and b. Ethylene oxide gas – interferes with dirty side in and hold it away from self. pathogen’s metabolic process. Disadvantages include toxicity to humans and duration of e. Respiratory etiquette exposure (1-6 hrs) Cover mouth and nose with tissue. Use upper sleeve c. Boiling water – practical and inexpensive but if not available. may be ineffective to some spores and viruses; boiling a minimum of 15 mins is advised for Transmission-based precautions – used in addition with standard home disinfection precautions. d. Radiation – UV rays, alpha, gamma, beta. a. Airborne precautions - used in measles, varicella, Disadvantage: rays do not penetrate deeply. tuberculosis, COVID (droplet mode but highly contagious) Ionizing rays (alpha, beta, x-rays) are best used Use negative pressure rooms with 6-12 changes to sterilize food, drugs, and other items per hour either discharge of air outside or with sensitive to heat. filtration system e. Liquid chemical sterilant – lengthy exposure time from 3-12 hours  Patients are placed in rooms near windows and Ex: Polyurases in farther from nurses station to prevent cross RTPCR and Nucleic contamination. acid amplification Cohort patients with same condition if there is test (NAT) room scarcity (pandemics) Interpretation of Antibody Test Results: Nurse wears N95 mask since pathogen has high *Highly sensitive isotopes: IgG (peaks 21 days to years) and IgM infiltration rate. (peaks from exposure up to 5 days or more of infection) Limit movement of patient to essential *Antibodies can still be present even if infection has passed. purposes. Let them wear surgical mask during *High IgG, low IgM – late or past infection transport. *High IgM, low IgG – early or active infection b. Droplet precautions – used in diphtheria, pneumonia, *Both increased IgG and IgM – active infection, previous infection, pertussis, mumps, rubella, scarlet fever or both Place clients in a private room. Cohort if not *Both IgG and IgM are low – pre-pathogenic infection, suggests available. early exposure to pathogen. Best time to give post-exposure Wear mask if working within 1 meter. Limit prophylaxis (48-72 hrs after exposure) client movement outside the room. Patient should wear a mask when required to Types of Immunity: leave the room. 1. Natural immunity – part of normal biologic process c. Contact precaution – for infections transmitted by direct 2. Artificial immunity – introduction of external substance contact such as GI, skin, respiratory or wound infections. Active Passive Skin infections such as impetigo, herpes, pediculosis, and Natural Recovery from a disease Placental antibodies scabies. triggers self- production and breastmilk Place client in private room or cohort. and memory of antibody Wear gloves. Change after contact with response infectious material, discard after leaving room. Artificial Vaccines and toxoids; Antitoxin and Handwashing immediately after removal. given to trigger antibody antiserums Wear gown before entering room. Remove production gown om the client’s room. Examples: TT vs TIG Infection Pathology: Tetanus toxoid – weakened toxin of Clostridium tetani Viral infection: Pathogen attaches and binds to target which will trigger antibody response. Given as a cell → release of viral proteins into the cell → prophylactic measure. Classified as artificial active combines with cellular proteins to replicate more viral immunity. proteins → formation of a “bulb” which will exit the cell Tetanus immune globulin – antibodies against tetanus. There is no need to activate production of antibodies). A and attack other healthy target cells → tissue damage treatment for exposure. Considered artificial passive → organ damage immunity. When attacked, cells perform apoptosis (cellular suicide) MAB (monoclonal antibody therapy) – artificial passive or pyroptosis (cell death d/t inflammatory process). immunity Antibodies prevent the pathogen from attacking target cells Types of Vaccines: Live attenuated vaccines – weakened actual pathogen is Antibody Isotopes (Immunoglobulins): introduced which develops better memory for antibody IgG (gamma) Most common type, usually found in the response making it the best which provides long-lasting blood (75%). The only antibody that crosses immunity. Usually a single-dose vaccine. (Ex: MMR, the placenta, giving immunity to the fetus rotavirus, smallpox, chickenpox) (natural passive immunity). Inactivated vaccines – killed or altered pathogens which IgA (alpha) Present in the mucus lining of the GI and cannot replicate. Considered as fastest, safest, and most respiratory systems to prevent attachment of common type of vaccine. Immunity is not long-lasting the pathogen. Present in saliva, tears, and and requires multiple doses and booster doses. (Ex: breastmilk (natural passive immunity) Hepatitis A, flu, polio, and rabies vaccines) IgM (macro) Largest antibody. Usually first to appear when Active components – introducing part or conjugate of an antigen is present (malaki ang mauuna). the pathogen (Ex: mRNA, structure proteins) IgE (epsilon) Involved in allergic response by binding to Toxoid vaccine – introducing the weakened toxin. allergens and trigger histamine release. Toxoid – inactivated toxin (Ex: DPT) Assists in parasite infection. Viral vector – introduction of a component of the virus IgD (delta) Not specific but with antimicrobial properties and injecting it to a safe virus or “vector” which the body has memory of. Trojan horse concept. (Ex: Diagnostic tests to determine presence and type of infection: Adenovirus, Ebola vaccine) (differ in sensitivity) COVID vaccines: NO live attenuated version Antibody Test Antigen Test Molecular Test Inactivated COVID vaccine – Sinovac, Bharat Biotech, Tests for presence Tests for presence Tests for presence Sinopharm of antibody of antigen of proteins (which Active component – mRNA-derived vaccines like Pfizer Not specific, only Not specific but are specific and Moderna checks for the can be used as a structures in the Viral vector – AstraZeneca, Gamaleya Sputnik-5, Janssen body’s response – confirmatory test pathogen. Most confirms presence for presence of specific test. of stimulation pathogens  Immunizable Diseases Chest x-ray – cannot detect active infection. Can only Tuberculosis detect fibrosis and parenchymal lesions. Used as Other names: Koch’s Disease, Phthisis, Consumption confirmatory test if with hemoptysis (since sputum Disease, Great White Plague sample cannot be used) Causative agent: Mycobacterium Preventive measures: BCG Vaccine, prompt treatment and Common in Asia and Africa (80% of cases worldwide) diagnosis, health education Management: Causative Agents: Airborne precaution – negative pressure room Tuberculosis types: Wear mask Mycobacterium tuberculosis - aerobic bacteria (oxygen- Px is communicable if not receiving antibiotic therapy. loving); attacks alveolar sac of the lungs Non-communicable after 24 hrs of 1st antibiotic dose but Mycobacterium africanus - common in West-African isolation is still advised up to 2 weeks from the start of countries. Symptoms are same as tuberculosis therapy. 3 successive (-) sputum – non-communicable Mycobacterium bovis - TB that infects cattle which can National TB Control Program – TB DOTS strategy; a be transmitted to humans via unpasteurized milk multi-drug therapy approach. Short treatment course Mycobacterium canettii - common in the horn of Africa: for about 6 months. Long course lasts from 9-12 Somalia and Ethiopia. Reservoir is unknown but months. Methods of administration: suspected in farm animals o Fixed dose – 2 or more anti-TB drugs are Mycobacterium microti - from rodents combined in one pill o Single drug formulation Non-tuberculosis type: Anti-TB drugs: (HRZES) all are strong antibiotics = Mycobacterium avium – from birds; usually hepatotoxic opportunistic, causes MAC (Mycobacterium avium o Isoniazid – neurotoxic and hepatotoxic complex) in AIDS. o Rifampicin – red-orange colored urine or body Mycobacterium kansaii – opportunistic, common in AIDS secretions Incubation period: 2-12 weeks o Pyrazinamide – hepatotoxic and MOT: airborne and droplet infection. Airborne precaution is used. hyperuricemia Manifestations: o Ethambutol – eyes impairment (optic neuritis): Low grade afternoon fever inability to see red or green colors Non-productive to productive cough for 2 weeks o Streptomycin – nephrotoxic and ototoxicity Chest pain effect Anorexia and weight loss Phases of TB Treatment Regimen: Description Intensive Maintenance Malaise and fatigue 1 + s/sx 2 mos RIPE 4 mos RI Night sweats + x-ray Hemoptysis New smear (+) or new smear (- Extra-pulmonary TB: spread into other organs (ex: GI tract, ) but with extensive pleura, meninges, lymphatic system, genitourinary, bones) aside parenchymal lesions from the lungs. Common in child and immunocompromised TB Extrapulmonary TB patients. 2 Relapse 2 mos RIPES 5 mos RIE Pathophysiology: Mycobacterium-containing droplet is inhaled → Treatment failure 1 mos RIPE 3 - s/sx 2 mos RIPE 4 RI alveoli are attacked → decreased respiration (respiratory + x-ray manifestations) → replication and inoculation in alveolar sacs → (asymptomatic) respiratory tissue damage → fibrosis of lung tissue and New smear (-), with minimal parenchymal lesions (lung opacities seen in chest x-ray) parenchymal lesions Diagnostics: 4 Chronic TB Refer to DOTS for 2nd line drugs Mantoux test – AKA tuberculin test or purified-protein derivative (PPD). Intradermal injection of 0.1 mL of PPD Leprosy into inner aspect of the lower arm. Result seen after 48- Other names: Hansen’s disease, Hansenosis, Leper’s 72 hours. Results based on induration. disease, Leontiasis o (+) TB: > or equal to 5mm induration if px is Causative agent: Mycobacterium leprae discovered in immunocompromised 1873 by Hansen. Found in armadillos who have a lower o (+) TB: > or equal to 10mm – healthcare body temperature workers, prisoners, children 4 y/o and below, A chronic infectious disease, majority contracted in travel to countries with high TB cases childhood and manifestations arise by 15-20 y/o. o (+) TB: > 15mm – general population Mode of Transmission: unknown but associated with direct o NOTE: BCG vaccine can cause false positive contact (droplet) – with prolonged close contact with a patient results with untreated leprosy DSSM – AKA C&S; confirmatory test for presence of Incubation period: 9 months to 20 years. Average: 5 years mycobacterium. Done under fluorescence acid fast Cardinal sign: cutaneous skin lesions, neuropathies in the hands microscopy staining by detecting and counting the and toes, sensory loss on the limbs presence of bacilli. o Sputum specimen collection: 3 specimens of at 2 classifications: least 5 mL sputum. Instruct patient to deep 1. Paucibacillary – tubercular type of leprosy with or less cough. Best time to collect in the morning skin lesions. Pauci = low quantity. o (+) TB: 2-3 positive sputum samples 2. Single lesion paucibacillary – 1 lesion only o If with 1 (+) specimen – repeat sampling and 3. Multibacillary – lepromatus type with 6 or more lesions testing o (-) TB: 3 negative specimen samples Pathophysiology: M. leprae replicate in cooler temperatures → invade areas with lower temperatures:  Skin infection: formation of white or reddish skin o airway obstruction → compromised nodules, loss of sensation in areas with lesions, non- respiration → barking cough and stridor to in healing ulcers, anhidrosis (inability to produce sweat) attempt to expel the obstruction → d/t damaged sebaceous glands, dry skin, hairless, loss of o hoarseness of voice eyebrows (madarosis) and eyelashes. o Increased inflammatory process → “bullneck” o Skin lesions form into large plaques and swelling in the throat nodules (common in earlobes, nose, Also affects other organs (heart) – toxic myocarditis, eyebrows, and forehead) = Leonine face neuritis, palate paralysis, ocular palsy, diaphragm Periphery: nerve damage causes atrophy of muscles in paralysis, motor, and skeletal muscle paralysis hands and toes causes: Diagnostic test: o claw-hand or radial-ulnar neuropathy Nasopharyngeal culture (stop antibiotics before culture) o claw toes or posterior tibial neuropathy – collect 2 swab samples with 24 hours interval o foot drop between. o muscle weakness → paresthesia PCR or ELISA – detect presence of diphtheria toxin o facial nerve paralysis → lagophthalmos (droopy eyes d/t paralysis of eyelids) → Prevention: DPT vaccine corneal infection and ulceration → blindness Management: Mucosa of URT: nasal perforation, saddle nose (collapse Isolate the patient and bed rest for at least 2 weeks. of the nasal bridge), epistaxis, ulcers in the uvula and Wear appropriate PPE (gloves and mask). tonsils Ice collar to reduce sore throat pain Diagnosis: Treatment of choice: Horse-serum based antitoxin or Skin or nerve biopsy – confirmatory test. Skin biopsy equine antitoxin which neutralizes the toxin. Nursing (CDC) or skin slit smear microscopy (WHO). 8mm of skin alert: conduct skin scratch test for allergies. sample is collected from the infected area with active Antibacterial agent: Erythromycin and Penicillin G for 14 lesions. days Prevention: BCG vaccine Pertussis Management: Highly contagious bacterial disease common among Multi-drug therapy – monotherapy will cause resistance children d/t immature immune function. Adults are WHO Treatment Protocol usually carriers of the disease o Paucibacillary – (-) skin smear. Give 600 mg Other names: Whooping cough, 100-day cough Rifampicin once/month + 100 mg Dapsone Causative Agent: Bordetella pertussis, B. parapertussis OD. Both are given for 6 months. Blister MOT: airborne or droplet pack/month = 6 blister packs IP: 4-21 days. Average of 5-10 days o Multibacillary – (+) skin smear with at least 5 Cardinal sign: whooping or explosive cough at night followed by a lesions. Give 600 mg Rifampicin once/month + sudden noisy inspiration with a crowing sound or “whoop”. During 300 mg Clofazimine once/month then 50 mg an attack, the child becomes cyanotic and with bulging eyes and daily + 100 mg Dapsone OD for 12 months = protruding tongue. 12 blister packs. Pathophysiology: o Single lesion – given single dose of 600 mg Stage 1: Catarrhal or Prodromal Stage (7-10 days) – manifests Rifampicin + 1 dose 400 mg Ofloxacin + 1 dose rhinorrhea, sneezing, low-grade fever, mild cough 100 mg Minocycline Stage 2: Paroxysmal Stage (1-6 weeks up to 10 weeks): episodes of o NOTE: Blister packs are released by WHO. worsened or whooping cough usually at night Cannot be bought in local pharmacies. Stage 3: Convalescent Stage (7-10 days up to 21 days): gradual recovery and reduced episodes of paroxysm Diphtheria Diagnostics: Other names: Bullneck disease, Klebs-Loeffler disease, Nasopharyngeal swab – only during first 2 weeks of pseudomembrane infection Characterized by generalized systemic toxemia from a PCR – during first 4 weeks of infection during the peak localized inflammatory focus of manifestations Site of infection: upper respiratory tract, specifically in Prevention: DPT vaccine - >90% effective in preventing the the tonsillopharyngeal area disease Causative agent: Corynebacterium diphtheriae or Klebs-Loeffler Management: bacillus Azithromycin, erythromycin, clarithromycin MOT: direct contact from an infected person, carrier, or infected Complications: pneumonia, seizures, encephalopathy d/t very low surfaces O2 Incubation period: 2-5 days Cardinal sign: pseudomembrane – smooth adherent whitish or Tetanus graying membrane attached on the hard palate Other names: lock jaw, sardonic smile disease, trismus Pathophysiology: entry into nasal cavity: Causative agent: Clostridium tetani – anaerobic bacteria nasal diphtheria) → nasal congestion with blood commonly found in the soil and manure. Spore-forming mucopurulent discharge lowers into bacteria carrying tetanospasmin toxin which causes tonsillopharyngeal diphtheria (most common site) → muscle spasms. sore throat and low-grade fever, chills, malaise, pain → MOT: direct or indirect contact. Enters the body via pseudomembrane formation d/t inflammatory response wounds or breaks in the skin. Can also happen in burns (WBC, fibrin, dead tissues) → pseudomembrane Incubation period: 3-21 days. Average of 10 days increases in size and spreads to lower respiratory tract Cardinal sign: lock jaw with trismus – muscle laryngeal diphtheria: contractions and spasms in the face Pathophysiology: C. tetani enters in low-O2 areas (wounds, burns) Diagnostics: → release of toxins (tetanospasmin) which causes muscle spasms 1. Lumbar Puncture – confirmatory test. 3 CSF samples → disrupts neuromuscular function starting on the face causing with 1 mL/tube each is collected. Result: glucose is low trismus and risus sardonicus (sardonic smile) → spreads in a and WBC count is increased in CSF: descending pattern → opisthotonos position → occurrence of Bacterial - > 100 WBC/mcL systemic spasms: sudden, powerful, lasting, and painful → risk for Viral 10-1000 WBC/mcL muscle tearing and bone fractures Fungal – 10-500 WBC/mcL Tetanus triad: trismus, sardonic smile, opisthotonos position 2. Blood culture Types of Tetanus: Prevention: Meningococcal vaccine (MenACWY and MenB) 1. Generalized tetanus – opisthotonos position; most Manifestations: common type (80%); affects the whole body with classic Meningitis triad: altered mental status, fever, nuchal manifestations rigidity 2. Localized tetanus – mild form and more common in Headaches partially immunized patients; spasms occur only on the Photosensitivity site of injury. Low mortality rate Kernig’s signs – with hips at 90, slow knee extension will 3. Neonatal tetanus – highest mortality rate. Common cause pain and resistance cause is umbilical infection. Full blow tetanus affects Brudzinski’s signs - batok flexion will activate knee immature neuromuscular system flexion upwards 4. Cephalic tetanus – rarest form caused by head injury. Complications: Manifestations include ptosis and unilateral facial Meningoencephalitis – altered mental state, seizures paralysis Management: Diagnostics: Depending on causative agent. Clinical presentation of symptoms Give antibiotics: cephalosporins (ceftriaxone, Spatula test: insert spatula until it reaches posterior wall cefotaxime) of the oropharynx. Normal = gag reflex. Tetanus (+) = Give corticosteroids to reduce inflammation spams occur and patient bites down on the spatula Prevention: DPT or Pentavalent Management: Influenza Tetanus immunoglobulin – single dose via IM route with AKA the flu; highly contagious acute viral upper 500 IU respiratory infection. Toxins impair ciliary action which Antibiotic – penicillin causes build-up of mucus in the airways. Muscle relaxants for spasms – benzodiazepines Causative agent: influenza virus Pain relievers and tranquilizers Types A – HN common in humans and animals (avian, Complications: fractures, respiratory paralysis (prepare bedside swine flu). Usually causes outbreaks. intubation set) Type B – seasonal flu common in humans only Type C – mild flu that is less common to adults. More Meningitis common in children Other names: cerebrospinal fever, Type D – common in cattle Inflammation of the meninges, particularly the first 2 MOD: droplet or contact transmission via contaminated objects inner layers (pia and arachnoid mater = leptomeninges), IP: 1-4 days. Average of 2 days caused by bacterial pathogens from either CSF or blood Mutation: Causative agent: NOT SPECIFIC TO ONE PATHOGEN, but Genetic mutation – genetic structure changes; commonly d/t bacteria: antibodies are not affected o Newborn: Streptococci, E. coli, Listeria Antigenic mutation – antigen structure changes; more monocytogenes. H. influenzae dangerous which will make antibodies useless upon o Children/Teens: N. meningitidis and mutation Streptococcus pneumoniae Pathophysiology: o Adults/Elderly: S. pneumoniae, L. Type A influenza carrying Hemagglutinin (18 kinds, used monocytogenes, M. tuberculosis to attach to the cell) and Neuraminidase (11 kinds, used o Viral: Enterovirus, herpes simplex virus, HIV to exit or bud from the cell) surface proteins = 198 o Fungal: Cryptococcus combinations, 131 are known to humans. o Parasite: P. falciparum Pathogen enters upper respiratory tract → pathogen MOT: droplet transmission via anatomical defect (e.g., spina attaches to endothelial cells on the mucosal lining with bifida, skull fracture) or hematogenous spread (blood infections H protein → release of viral proteins → replication of like malaria) viral proteins → release and exit with N protein → new IP: 2 days to 2 weeks depending on causative agent viral cell infects other healthy cells. Coughing, sneezing, talking can transmit virus to other 2 types: people 1. Primary – spread of bacteria from the bloodstream to General Prevention: meninges Avoid sick people with the disease 2. Secondary – results from direct spread of infection from Frequent and proper handwashing other sources Cleaning and disinfecting surfaces Pathophysiology: entry of pathogen from direct contact or Vaccine: annual flu vaccine as early as 6 mos. old hematogenous spread → bloodstream infiltration → entry into Indicated for those > 50 y/o or immunocompromised the blood brain barrier → replication of pathogen in CSF → individuals. Yearly vaccine since there are multiple inflammation of leptomeninges → increased WBC count in CSF (N strains to the influenza virus = 1 microliter:5 WBC count) → meningoencephalitis → encephalitis → coma Avian Influenza A (H5N1) o ALT (Alanine transaminase) – more specific Affects birds and does not usually affect humans. Birds indicative of liver damage are migratory in nature. o AST (Aspartate transaminase) – may also H5N1 vaccine is developed and ready for use indicate muscle damage (ex: heart). Prevention: thorough cooking of poultry, avoid contact with wild IgM – elevated during early acute infection animals IgG – found in the blood; elevates during convalescent Swine Influenza (H1N1, H1N2, H3N1, H3N2) stage AKA Spanish flu Management: Strain of flu from genetic material from swine, avian, Supportive treatment and human flu virus Bed rest S/sx is same with seasonal flu with addition of vomiting Prevention and diarrhea Hepatitis A vaccine – inactivated type. 2 doses: 12-13 Manifestations: mos. (1st) and 6 mos. after 1st dose (2nd dose). 0.5 mL via Acute onset of fever and myalgia IM. Precautions: apply contact precautions and proper Headache waste disposal of diapers and tissues Fatigue, weakness, anorexia Sore throat, non-productive cough, rhinorrhea Hepatitis B Diagnostics: AKA serum hepatitis – acute condition that can lead to a RIDT – rapid influenza diagnostic test; result in 15-30 chronic infection mins. Detects the type of influenza CA Hepatitis B virus – double strand DNA virus PCR – swab sample detects the actual viral protein MOT Blood transmission – sharing of contaminated (confirmatory test) needles, sexual transmission, perinatal transmission Management: IP 60-150 days (average: 90 days) Severe case: Diagnostics: o Neuraminidase inhibitors such as OseHamivir Polymerase Chain Reaction – used as a viral load or Peramivir. indicator o M2 proton inhibitors AKA adamantanes which Specific serum markers: prevents replication by inhibiting attachment o HBsAg (Hepatitis B surface antigen) – detects to endothelial cell membrane. Ex: presence of Hepa B virus; first serum marker Amantadine, Rimantadine to appear and detectable prior to onset of Rest. Encourage fluids. Monitor lung sounds. Supportive symptoms. Peaks at 12 weeks of infection and therapy such as antipyretics and antitussives. undetectable after 6 mos. Used to confirm Administer antivirals as prescribed. immunity with Hepa vaccines (low HBsAg if immune) Hepatitis o HBeAg (Hepatitis B E antigen) – detects viral Inflammation of the liver replication. High levels = high replication rate Causes: = high viral load = highly transmissible during Drugs and medications childbirth. Detectable between 6-14 weeks of Excessive alcohol intake infection Viral infections o HBcAb (Hepatitis B Core antibody) – first antibody to be detected Functions of the Liver: o HBeAb (Hepatitis B E antibody) – fights 1. Bile production – helps in the absorption of fats, HBeAg; high levels = low viral load cholesterol, and fat-soluble vitamins Management: 2. Absorption and metabolism of bilirubin which comes Pegylated Interferon (Pegasys) – nucleoside drug from breakdown of Hgb from RBCs. Naturally brownish Antivirals – Lamivudine, Adefovir, Entecavir, Tenofovir in color. In hepatitis, bilirubin leaks into the system and (similar to HIV) causes jaundice as well as clay-colored stools Condition is curable but not easy and takes a long time 3. Blood clotting – Vitamin K storage which are necessary Prevention: in production of coagulants Hepatitis B vaccine – active recombinant. With 3 doses: 4. Carbohydrate metabolism and storage in the form of 1st – at birth, 2nd – 1-2 mos. 3rd – 6-18 mos. old. glycogen which is used for energy < 20 y/o – 0.5 mL 5. Vitamin and mineral storage – ADEK vitamins and Vit. Adults – 1 mL via IM route. B12 Brand names: Engerix B, Recombivax HB 6. Breakdown of proteins – byproduct is ammonia → urea Precautions: which is more soluble Blood borne precautions 7. Filters the blood – portal circulation Safe sex practices Hepatitis A Hepatitis C AKA infectious hepatitis, catarrhal jaundice AKA non-A, non-B hepatitis, inoculation hepatitis An acute infection that can last for < 6 months Acute and/or chronic infection CA Hepatitis A virus – single strand RNA CA Hepatitis C virus – single strand RNA virus MOT Fecal-oral route MOT blood transmission – sharing of contaminated IP 15-50 days with an average of 28 days needles, sexual transmission, perinatal transmission Diagnostics: IP 14-180 days (average: 45 days) Liver enzymes: helps in detecting damage in liver Diagnostics: tissues. Damage = high levels of liver enzymes Can reveal normal liver enzymes Hepatitis C antibody test  PRC – confirmatory test Note: Hepa B can also transcribe to SSRNA to combine with host Management: cell’s RNA (follows single stranded RNA virus pattern) Pegylated Interferon (Pegasys) + Ribavirin Direct-acting antivirals such as combo drug of Stages of Hepatitis: Elbasvir/Grazoprevir, Ledipasvir/Sofobuvir 1. Prodromal stage – with viremia (virus present Prevention: in blood circulation). With fever, headache, No specific vaccine yet but may use vaccines against anorexia, nausea, fatigue Hepa A and B 2. Icteric stage – with damage of liver and Precautions: release of pathognomonic s/sx: jaundice, dark Blood borne precautions urine, gray colored stools, yellow sclera, Safe sex practices hepatomegaly Complications: 3. Convalescent stage – recovery stage and Liver cirrhosis return to normal liver size. With increased Hepatocellular carcinoma appetite, decreased jaundice, normal colored excreta Hepatitis D Note: AKA co-infection hepatitis (requires Hepa B precursor) Recovery of the patient depends on severity, not the Classified as chronic infection only type of hepatitis. 2 types: Undetected – means that viral load is not sufficient to Co-infection – together with Hepa B be detected in the test but does not mean that the disease is not there. Super-infection – Hepa B progresses to Hepa D infection Missed dose – administer immediately and continue CA Hepatitis D virus – single strand RNA virus with normal interval MOT blood and blood-products transmission IP Co-infection: 45-160 days (average: 90 days) Superinfection: 2-8 weeks Diagnostics: Hepa B serum markers PCR to detect viral load Management: Pegylated Interferon (Pegasys) – nucleoside drug Prevention: No specific vaccine yet but may use vaccines against Hepa B Precautions: Blood borne precautions Hepatitis E AKA perinatal hepatitis since the common at-risk population are pregnant women An acute infection only CA Hepatitis E virus – single strand RNA virus MOT Fecal-oral transmission IP 15-69 days (average: 40 days) Diagnostics: PCR to detect viral load Management: Ribavirin Precautions: apply contact precautions and proper waste disposal of diapers and tissues Complication: Fulminant Liver Failure – too many affected liver cells renders liver unable to function Pathophysiology (shared by all types of Hepatitis) Hepa A, C, D, E – single strand RNA attacks liver cells or hepatocytes → binding and attachment → release of single strand RNA into the hepatocytes → combine with the host’s own RNA – polymerases of cells → results to more viral RNA → replication and release out of the hepatocyte → invades other healthy hepatocytes → lysis of hepatocytes → apoptosis (cell death) → tissue necrosis → cessation of liver functions Hepa B – double strand DNA attacks liver cells or hepatocytes → binding and attachment → transcription and combination of DNA of the host cells → replication and release → more viral DNA invade other hepatocytes ADDITIONAL NOTES: Blood and Vector-borne Disease COVID 19 Pathophysiology – virus attacks the alveolar sacs /Dengue which are lined by pneumocytes which are responsible for gas /Malaria exchange → impaired gas exchange → poor oxygenation /Filariasis /Leptospirosis Delta vs Omicron Variant: Delta – attacks LRT making it more fatal; incubation CNS Communicable Disease period is 3-9 days Omicron – attacks URT; more communicable and /Meningitis with shorter incubation period (2-5 days) Meningococcemia /Rabies Cardinal signs: Poliomyelitis Dentations/ulcers (donut-shaped) – small-pox / Tetanus With a dot in the lesion – Bacillus anthracis (anthrax) Erythema infectiosum – slapped cheek and lacy erythema Hepato-enteric Diseases Schistosomiasis Creutzfeldt-Jakob disease – unknown reasons causes an Typhoid fever abnormal misfolding prions (protein-structures) inside the /Hepatitis neurons which are seen as foreign organisms → inflammation Ascariasis or apoptosis → spongiform encephalopathy. Roundworm Tapeworm Mad Cow Disease – bovine-spongiform encephalopathy caused Flatworm by ingestion of abnormal prions from unpasteurized milk Pinworm SARS vs MERS Eruptive Fevers Both come from bats. MERS is from Egyptian tomb / Measles (Rubeola) bats which infected camels to humans. German Measles (Rubella) Chickenpox (Varicella) Portal of Entry vs Portal of Exit: Smallpox Entry – a part of the body (hole or cavity) that allows Kawasaki Disease infectious agent to enter the body / Diphtheria Exit – body fluid that is secreted from the portal of / Whooping Cough entry / Pulmonary Tuberculosis Pneumonia Clostridium difficile – drug-related infection caused by strong Scarlet Fever antibiotics which destroys normal flora; commonly happens in Shigellosis elderly. Not removed by alcohol-based hand rub. Needs soap Cholera and water handwashing. Gloves must always be used. Botulism / Leprosy Antiretroviral drugs – non-nucleoside and nucleosides, / Influenza protease inhibitors; interfere with the viral replication process but not directly killing the virus Sexually Transmitted Diseases /Gonorrhea EO 51 – Milk Code: provides other options aside from /Chlamydia breastmilk /Syphilis RA 7600 – Breastfeeding and Rooming In Act: highly /Herpes Genitalis encourages breastfeeding which can last up to 2 years and /Genital Warts beyond, but should be exclusive for the first 6 months /Candidiasis /Trichomoniasis Meningitis vs Meningococcal Disease vs Meningococcemia /HIV/AIDS Meningitis – inflammation caused by any causative agent. Meningococcal Infection – caused by Neisseria meningitidis. With types A, B, C, W, X, Y. Meningococcemia – infection of the meninges and septicemia Stool Manifestations: Giardiasis – steatorrhea Dysentery and amebiasis – bloody stool Cholera – profuse watery stool  Mosquito-Borne Conditions initially increased BP → continuous bleeding → low BP with Aedes Anopheles Culex continuous bleeding → hypovolemic shock → coma → death Disease Dengue, Zika, Malaria Japanese Chikungunya, encephalitis Diagnostics: Yellow fever West Nile 1. Tourniquet or Rumpel-Leads or Capillary Fragility Test Disease A presumptive test for dengue that is applicable only Active Hours Aggressive Dawn and Dawn and during febrile phase. Can give a false positive result day biters dusk. More dusk. Active during toxic stage active at at night Measure coagulability of the blood – assess bleeding night tendencies Flying Low flying High flying Contraindicated in px with fistulas, AV shunt and post- (common in mastectomy forests) Apply sphygmomanometer on the upper arm and inflate Features Black and Dark legs, Tan colored BP cuff midway between systolic and diastolic BP for 5 white, dark thorax, thorax with mins. Release cuff and measure a 1-square inch at the striped legs, spots in the striped dark antecubital fossa. Inspect and count # of petechiae. lyre thorax wings legs and dark (+) = 20 or more petechiae wings 2. Capillary refill test or nail blanch test – measures dehydration Ecology Stagnant Ponds and Polluted and decreased peripheral perfusion. N = less than 3 seconds. water lakes water 3. Platelet count and Hct count – confirmatory test Sound Less sound Peculiar, loud (+) dengue: decreased platelet count and increased Hct sound count → suggests progress to critical phase Resting Parallel 45-degree Parallel 4. Coagulation parameters position angle 5. Dengue rapid test – tests for the dengue virus antibody (IgG and IgM) Dengue Hemorrhagic Fever AKA breakbone fever, dandy fever, infectious Dengue Case Classification: thrombocytopenic purpura Probable Travel or lives in endemic area An acute infectious mosquito-borne fever marked by Fever and 2 of the ff criteria: extreme pain and stiffness of the joints N/V Common during the rainy season and in congested, Rashes urbanized areas epidemic in populated areas with poor Aches and pains environmental sanitation (+) tourniquet test All individuals can be affected but more common in Leukopenia children from 0-9 y/o. Any warning sign CA Dengue virus – single stranded RNA virus with 4 Warning Signs Abdominal pain/tenderness – s/sx of GI major serotypes (DEN 1-4) from the genus Flavivirus. bleed A person can get dengue 4 times since there is no Persistent vomiting cross-immunity between the types. Clinical fluid accumulation MOT Vector – through a mosquito bite. Female Aedes Mucosal bleeding feeds on infected person → virus infects Aedes’ Lethargy/restlessness midgut and spreads systematically for 8-12 days → Hepatomegaly > 2 cm infectious bite to a healthy person Increased Hct with decreased platelet count IP 3-14 days, average of 5-7 days Severe Severe plasma leakage leads to: Vectors: Dengue Shock – dengue shock syndrome 1. Female Aedes aegypti mosquito – primary vector Fluid accumulation with respiratory AKA yellow fever or tiger mosquito. distress Common in tropical and subtropical countries. Severe bleeding Proliferates in clear, stagnant water (domestic water Severe organ involvement storage or rain-filled habitats) Liver AST or ALT > 1,000 Feeds at dusk, before sunset, dawn and just after CNS: impaired consciousness sunrise when indoors (day-biters) Heart and other organs 2. Aedes albopictus – AKA Asian tiger mosquito. The secondary Phases of Dengue Illness vector, predominant in rural areas and common outdoors. 1. Febrile Phase – 1-3 days. Manifested by high-grade Found in leaves, tree holes, bamboo stumps. Transmits fever (39 degrees and up), convulsions, (+) Tourniquet chikungunya virus test, anorexia, facial flushing, skin erythema, myalgia, 3. Aedes polynesiensis - found in other countries arthralgia, and headaches, abdominal pain. Mild 4. Aedes scutellaris – found in other countries hemorrhagic manifestations (petechial rashes, gum bleeding, and nosebleeds) are seen. WOF warning signs Reservoir: humans, monkeys (West Africa and SE Asia) closely to identify entry to critical phase. 2. Toxic/Critical/Hemorrhagic Phase – 1-2 days; Pathophysiology: temperature drops and remains below 37.5-38 C. Entry of dengue virus through skin inoculation → infected restlessness with cold and clammy skin. Increased Hct macrophages → manifest flu-like symptoms → infection of the levels and rapid decrease in platelet count occurs blood stream which circulates around the system → increased (precedes plasma leakage). Pleural effusion and ascites viral load d/t replication, especially the bone marrow → may occur. Shock may occur which if prolonged can lead decreased platelet production (20,000 and even lower) → clotting to organ damage, metabolic acidosis, and DIC. factors is decreased → bleeding → tachycardia to compensate →  3. Recovery Phase – 8-10 days. General well-being Dengue Vaccine – Dengvaxia by Sanofi. It is a live recombinant improves, appetite returns, and hemodynamic status tetravalent vaccine for all 4 types of dengue. License was revoked becomes stable. by February 2019 due to side effects. Dengue Class according to Severity (Halstead-Ninmanitya) Malaria Grade 1 Dengue fever AKA marsh fever, periodic fever, king of tropical Saddleback fever – biphasic fever with 2 peaks diseases, black water fever Constitutional s/sx Marked by RBC destruction, hypertrophy of the spleen (+) tourniquet test and liver, and pigmentation of organs d/t phagocytosis Grade 2 Grade 1 plus spontaneous bleeding, epistaxis, GI of malarial pigments that are released into the blood or cutaneous bleeding stream upon rupture of RBCs Grade 3 Dengue shock syndrome – with evidence of Endemic in Palawan and Mindoro circulatory failure Grade 4 Grade 3 plus irreversible shock and massive CA Plasmodium protozoan species bleeding P. falciparum as the most dangerous and common in the Philippines. Causes malignant Nini’s Grading Shortcut: tertian malaria 1 __ Flu s/sx + Tourniquet test P. vivax – widely distributed, 2nd most common. 2 1 + Bleeding (epistaxis, abdominal Causes tertian malaria bleeding, gingival bleeding) P. knowlesi – zoonotic malaria (monkeys in SE 3 2 + 500 cells/mm3 (able to fight other direct contact of open wounds/mucous membranes infections) with contaminated blood, body fluids, semen, and CD4 or T-cell Count vaginal discharges, mother to fetus transmission N = 500-1,500 cells/mm3 through placenta, delivery, or breastmilk > 500 cells/mm3 – can fairly fight against other IP Variable – 3-6 mos. to 8-10 years infections but diseases like TB can be more common Note: more deaths are associated with HIV 2 since research and and severe treatment are leaning to HIV 1 200-500 cells/mm3 – causes lymphadenopathy and hairy leukoplakia (white patches on the tongue HIV History caused by Epstein-Barr virus), and oral candidiasis 1981 – first case of HIV in USA with manifestation of < 200 cells/mm3 – AIDS; with persistent fever and Pneumocystis pneumonia fatigue, weight loss, diarrhea. HIV viral count Incidence rate: 84% of cases from male-male sexual increases significantly transmission, 11% from heterosexual sex, 4% from sharing infected needles, 1% via vertical transmission, blood, HIV Viral Load transmission and other Measure # of HIV copies in mL of blood; assess Incidence: more common in African Americans, males, progression of HIV disease homosexuals aged 20-40 y/o Undetectable viral load = px is no longer infectious. Female with undetectable viral load can get pregnant HIV (+) and a (-) sex – sero-discordant relationship. Negative and breastfeed person still be HIV free as long as HIV (+) has undetectable viral < 20-75 copies/mL – acceptable levels; good loads and compliant with ARTs. < 200 copies/mL – stable but monitoring is essential  > 200 copies/mL – requires medical attention and Philippines: with treatment hubs with established HIV/AIDS core drug therapy team (HACT) Services include prevention, treatment, and care Acquired Immunodeficiency Syndrome services Most severe stage; with high viral load and infectious Case management and monitoring Highly immunocompromised – risk for opportunistic HIV counseling and testing infection Provision of antiretroviral drugs Not a disease but a syndrome – state of the body With community support organizations (ex: Pinoy Plus acquired due to an immunodeficiency (immune-less Association, Positive Action Foundation Philippine) state) 4 Cs in Case Management: Defining Characteristics: Compliance of clients Endocrine abnormalities Counseling and education P. Carinii pneumonia Contact tracing Protozoan infection – Pneumocystis jiroveci pneumonia Condom use Lymphadenopathy for at least 3 mos. leukopenia Neurologic impairment Lymphoma Recurrent bacterial pneumonia Fungal infections – candidiasis, histoplasmosis Kaposi’s sarcoma – purplish-red lesions in internal organs and skin Diagnostics for HIV AIDS: Window period – early stage of infection wherein a person has HIV but tests negative d/t insufficient antibody count. Usually between 3-12 weeks Antibody test – rapid or self-test kits Antibody-antigen test – detect both antibodies and the virus itself. Enzyme-linked immunosorbent assay (ELISA) – if positive, it is followed by Western blot to confirm HIV. Test is recommended for people who use IV drugs, unsafe sex practices, previous STDs, and blood transfusions. This test can elicit false positive results in px with Lyme disease, syphilis, or lupus. RNA/DNA test (Western Blot) – confirmatory test Management: Antiretroviral therapy (ART) – single or combination HIV regimen which interfere with the viral replication process but not directly killing the virus Non-nucleoside reverse transcriptase inhibitors – turn off proteins needed by HIV to replicate. Ex: efavirenz, rilpivirine, and doravirine Nucleoside Drugs – faulty versions of building blocks needed by HIV to replicate. Ex: abacavir, zidovudine, tenofovir, emtricitabine, and lamivudine Protease Inhibitors – inactivate HIV protease. Ex: atazanavir, darunavir, and lopinavir. Others: Respiratory support – O2 therapy Psychosocial support F&E balance WOF signs of infection. Initiate reverse isolation precautions Nutritional support Prevention: Blood: Screening of blood donors and use of universal precautions. Refrain use of contaminated or used needles Sexual transmission: abstinence, monogamous sexual contact, use of condoms Mother to child: consult with HCW for care, treatment, and delivery methods Stages of HIV: Cryptococcus – yeast infection caused by a Cryptococcus Stage 1A Primary Infection or Acute HIV Syndrome neoformans. Occurs when CD4 count is very low. Can last for 2-4 weeks, 1-3 weeks Mgmnt: Fluconazole and Amphotericin B CD4 cells begin to decrease – lower than Cryptosporidiosis – a diarrheal infection caused by 1,500 cells. Normal count is 500-1,500 protozoa Microsporidiosis. Mgmnt: Nitazoxanide or cells/mm3 Paromomycin. Goal is to increase CD4 levels through S/sx: flu-like symptoms, night sweats, anti-retroviral drugs fatigue, headaches, persistent When CD4 is < or = 50 cells: generalized lymphadenopathy Cytomegalovirus (CMV) – can spread and infect other Stage 1B HIV Asymptomatic organs. Exhibit retinitis, esophagitis, colitis, encephalitis. “dormant stage” and virus stays in lymph Mgmnt: Ganciclovir or Foscarnet nodes Mycobacterium avium complex (MAC) – a non-TB May last from 2-10 years mycobacteria that does not affect healthy individuals CD4 cell – 500 cells and above but affects severely immunocompromised. Mgmnt: S/sx: persistent generalized Azithromycin or Clarithromycin + Ethambutol lymphadenopathy. No major Bacillary angiomatosis – caused by Bartonella henselae manifestations that can last from 8-10 or Bartonella quintana. Marked by reddish-purplish rash years with nodules in the skin. Mgmnt: Erythromycin, Stage 2 Symptomatic Doxycycline, Azithromycin CD4 count = 200-499 cells/mm3 S/sx: bacillary angiomatosis, candidiasis, Diagnostics: cervical dysplasia, fever (38.5 C and Note: CDC recommends frequent screening for: above), diarrhea (for 1 month and more), Population ages 13-64 y/o at least once/year hairy oral leukoplakia (oral thrush), For at-risk populations at least 1x/year shingles (herpes zoster), PID, peripheral Sexually active, gays, bisexuals tested every 3-6 months neuropathies Stage 3 Acquired Immunodeficiency Syndrome Tests include: Stage of severe immunodeficiency status Enzyme Link Immunosorbent Assay Test (ELISA) – d/t pyroptosis and apoptosis of CD4 cells screening test CD4 cell count = 200 cells/mm3 and Western Blot – confirmatory test below + opportunistic infections CD4 count Viral load Opportunistic Infections: Nucleic Acid Test – can detect HIV infection as early as Any CD4 count: 10-33 days Tuberculosis of any type – may include extra-pulmonary Goal: Increased CD4 count, and viral load should be undetectable. TB Undetectable is untransmissible. Does not mean that there is no Oral candidiasis - CD4 = 200-500 cells/mm3. Mgmnt: infection but indicates that replication of the virus is minimal Fluconazole PO which makes transmission difficult. Kaposi’s sarcoma – a type of cancer caused by human Free testing is available in sanitary clinics. herpes virus 8 (HH8) manifested by reddish-purplish- Superinfection occurs when a person has both types of brownish-black papular lesions on the skin that are HIV. slightly elevated from the skin. AIDS-defining illness. Common in CD4 count < or = 250 cells/mm3 Management: Coccidioidomycosis – fungal infection common when Post-exposure Prophylaxis (PEP) - taken 73 hours after CD4 < or = 250 cells. Mgmnt: Fluconazole daily until CD4 an exposure to prevent HIV inoculation. Taken daily for is above 250 28 days. Includes a combo of 2 drugs: Tenofovir + When CD4 < or = 200: (AIDS) Lamivudine or Emtricitabine Bacterial pneumonia – prevention includes PPSV 23 Pre-exposure Prophylaxis (PREP) – advisable as vaccine (Pneumovax) given every 5 years maintenance for highly sexually active individuals. Pneumocystis pneumonia – CA is a protozoa Brands available: Truvada (sky-blue, white is an ARV), Pneumocystis jirovecci. Mgmnt: Trimethoprim or Descovy (not approved for women). Sulfamethoxazole o Taken daily for 7 days to be effective in MSM. Isosporiasis – SKS cystoisosporiasis; watery, non-bloody o Taken for 20 days to be effective for vaginal diarrheal illness caused by protozoa Cystoisospora belli. Mgmnt: Cotrimoxazole sex When CD4 < or