Clin Med Exam 1 PDF

Intro to Infectious Disease Nicole Scovazzo, EdD, PA-C Physician Assistant Studies PAS 521: Clinical Medicine I Lecture Objectives Differentiate between colonization and infection Differentiate between various types of infections Identify various pathogens that c...

Intro to Infectious Disease Nicole Scovazzo, EdD, PA-C Physician Assistant Studies PAS 521: Clinical Medicine I Lecture Objectives Differentiate between colonization and infection Differentiate between various types of infections Identify various pathogens that cause infectious diseases Summarize methods of preventing spread of infectious diseases Discuss host defenses against infection Classify laboratory tests utilized to identify infectious agents Discuss the management of infectious diseases Identify emerging challenges in infectious disease ID Terminology Disease - any disturbance in the structure or function of the body Infectious Disease - disease caused by a pathogen Pathogen – microbe that causes disease in a host Colonization - presence of a microorganism on or in a host without disease Infection - presence of a microorganism on or in the body that results in signs and/or symptoms Primary Infection - infection in a person who was previously healthy Secondary Infection - occurs during or after treatment for another infection antibiotics causing a yeast infection Opportunistic Infection - infections that occur more often or are more severe in individuals with weakened immune systems Health care-associated (nosocomial) infection - infection acquired while receiving health care that was not present during the time of admission UTI from catheter AccessMedicine > Review of Medical Microbiology & Immunology: A Guide to Clinical Infectious Diseases, 17e > The Human Microbiome Warren Levinson, Peter Chin-Hong, Elizabeth A. Joyce, Jesse Nussbaum, Brian Schwartz Types of Infections Acute: pathogen causes illness of relatively short duration with rapid recovery formement illness occurs for a long time Examples: UTI, influenza Chronic/Persistent: pathogen can be continually detected; host may or may not demonstrate symptoms Examples: H. pylori, hepatitis Latent: pathogen lives hidden within the host without producing clinical signs or symptoms. This type of infection can reactivate Examples: Tuberculosis, Varicella Subclinical: infection with pathogen capable of producing disease but host has no detectable symptoms Examples: Group A strep, SARS-CoV-2 Pathogens Bacteria Viruses Fungi Parasites Protozoa Helminths worms Prions abnormal proteins in the brain Classification of Bacteria Gram Staining th Morphology shape Oxygen aerobic anaerobic Gram Staining Positive Negative Gram stain = BLUE Gram stain = RED Thick peptidoglycan layer Thin peptidoglycan layer Low lipid content Outer membrane with lipopolysaccharide Secrete exotoxin from bacteria antigenic Less likely to make exotoxin No endotoxin unique tobacteria Endotoxin Vulnerable to lysozyme and penicillin/beta-lactam antibiotics Resistant to lysozyme and cephalosporins penicillin stimulate immune system Exotoxins Proteins secreted by bacteria More often come from Gram + bacteria Can cause severe disease 0 Bioterrorism agents (ex: Bacillus anthracis ) Types Neurotoxin nerves CNS Enterotoxin Gl Pyrogenic toxins inflammation fever Tissue invasive toxins necrosis oftissue Endotoxins Lipopolysaccharide membrane compounds Component of gram O – bacteria Causes severe illness if enters bloodstream on High fever Shock Disseminated intravascular coagulation DIC critical stressor causes clotting and bleeding at the same time Morphology Gram Positive Bacteria 3 cocci 3 non-spore forming rods Streptococcus grows in Corynebacterium dip theria strips chains Staphylococcus Listeria food poisoning grows in groups clusters Enterococci Actinomyces skin disease 2 spore forming rods Bacillus anthrax Clostridium tetanus botulismgangrene Strep Staph Gram positive Streptococcus Group A β-hemolytic streptococci (GABHS)strep pyogenes Pharyngitis Strep throat Scarlet fever Rheumatic fever Impetigo skin infection yellow crusting ENT infections Pneumonia strep pneumonia Toxic shock syndrome Various skin and soft tissue infections Erysipelas Cellulitis Necrotizing fasciitis Staphylococcus Aureus Clinically important bug MRSA especially concerning resistant to antibiotics ooo Skin and soft tissue infections Musculoskeletal infections Infective endocarditis Bacteremia Toxic shock syndrome Nosocomial or ventilator associated pneumonia Device related infections Gram Negative Bacteria Almost all the rest Only 1 gram-negative coccus (actually a diplococcus) gonorrhea or Neisseria meningitis c Remainder are pleomorphic coccobacilli or bacilli Gram Negative Bacteria Enteric doesn'talwayscauseinfection where it lives Pathogenic inside and outside of GI tract Escherichia, Salmonella Pathogenic primarily inside GI tract Shigella, Vibrio, Campylobacter, Helicobacter Pathogenic outside GI tract Klesbsiella, Enterobacter, Pseudomonas, Proteus, Serratia, Bacteroides Respiratory Haemophilus, Legionella, Bordetella Animal sources Yersinia, Pasteurella fathmans  cultures take minimum 48hours Gram…..????? Spirochetes So small they can only be seen on darkfield microscopy Treponema, Borrelia, Leptospira syphilis lyme leptospirosis Atypical bacteria TB Mycobacteria & Nocardiaendocarditis Lipid-rich cell wall, make it resistant to Gram staining so Identified with acid fast staining, culture Mycoplasma No cell wall, so nothing stains Diagnosis: cold agglutinin test, DNA probe, culture Obligate Intracellular Bacteria Cannot survive without a host gramstain or grow in cultured Candt Chlamydia Rickettsia RMSF tickborne Oxygen Preferences Some bacteria have enzymes that can break down the byproducts of O2 metabolism Some don’t have to test differentforaerobicandanaerobiccultures Categories Obligate aerobes Obligate anaerobes Facultative anaerobes Aerotolerant/microaerophilic willgrow a little aerobic grow faster anaerobic Viruses Typically smaller than bacteria Obligate intracellular pathogens Cannot replicate without a host Carry the enzymes they need to replicate Nhfnucleus Consist of Proteins Capsid Internal proteins Envelope Genetic material Classification of Viruses Nucleic Acid Envelope RNA Non-enveloped virus weaker +, - or retroviruses DNA Enveloped disrupt Confers instability Ifr Have + and - strand Size Capsid shape Number of capsomers in Icosahedral icosahedral capsid Most DNA viruses Diameter of helical capsid Helical Most RNA viruses  ᵈ of Clinically Important Viruses RNA DNA Coronavirus Human herpesviruses Hep A virus Parvovirus Hep C virus Norovirus Human papillomavirusHPVwarts Rotavirus Poxvirus Rhabdovirus Adenovirus Influenza virus Hep B virus HIV Paramyxoviruses Transmission of Infectious Disease Source: Centers for Disease Control and Prevention. Principles of epidemiology, 2nd ed. Atlanta: U.S. Department of Health and Human Services;1992. Chain of Infection Pathogen Bacteria Fungi Viruses Parasites Prions Reservoir People Susceptible Water Host Soil Food Animals/Insects Portal of Entry Portal of Exit Mucous membrane Blood Respiratory Secretions Urogenital Excretions GI Mode of Skin Broken Skin Transmission Contact Droplet Airborne Vector Vehicle  Antimicrobial Therapy Disinfection Sterilization Immunizations Health maintenance Pathogen Treatment of Disease Recognition of high risk patients Prophylaxis Susceptible Reservoir Host Water treatment Proper food storage BREAK THE Environmental controls/sanitation Hand hygiene CHAIN Aseptic technique Catheter care Wound care PPE Portal of Portal of Exit Entry Hand hygiene Control of excretions Mode of and secretions PPE Hand hygiene Transmission Trash & waste disposal Proper food handling Isolation Air flow control PPE Phases of Infectious Disease Incubation period: time between infection and the onset of signs and symptoms Prodromal phase: period of mild, nonspecific symptoms Constitutional symptoms fatiguemalaisefever Clinical phase: patient presents with signs and symptoms specific to disease nausea vomiting diarrhea cough congestion Decline phase: signs and symptoms begin to subside Recovery phase: symptoms are gone, tissues heal and the body’s function returns to normal  Host Defenses: Innate Immunity (First Line) Physical, Chemical and Biological Barriers AccessMedicine > Review of Medical Microbiology & Immunology: A Guide to Clinical Infectious Diseases, 17e > Innate Immunity Warren Levinson, Peter Chin-Hong, Elizabeth A. Joyce, Jesse Nussbaum, Brian Schwartz Host Defenses: Innate Immunity (Second Line) “Quick” immune response to invasion of or injury to our cells No memory and nonspecific Phagocytic cells and inflammatory response very important Three key jobs: 1. Itstepin fighting infection control Recognize invaders, kill them and recruit help 2. Contain infection to local site of inflammation causesedema 3. Help repair the damaged barrier Host Defenses: Adaptive Immunity (Third Line) Slower immune response that has a memory Highly specific Cell-mediated immunity (T cells that attack antigen) Humoral immunity (B cells that turn into plasma cells and produce antibody to the antigen)  mature Esen heart phagocytosis neutrophils killer cells Schematic diagram of the cellular interactions in the immune response. Citation: Chapter 8 Immunology, Riedel S, Hobden JA, Miller S, Morse SA, Mietzner TA, Detrick B, Mitchell TG, Sakanari JA, Hotez P, Mejia R. Jawetz, Melnick, & Adelberg's Medical Microbiology, 28e; 2019. Available at: https://accessmedicine.mhmedical.com/content.aspx?sectionid=217769996&bookid=2629 Accessed: December 31, 2020 Copyright © 2020 McGraw-Hill Education. All rights reserved Immunocompromised Hosts Increased risk of infection with common and opportunistic pathogens Defenses are broken down at some or all levels Primary Immunodeficiency Rare Typically a result of genetic defect Can involve innate or adaptive immunity Innate system is less commonly affected https://accessmedicine.mhmedical.com/ViewLarge.aspx?figid=227559260 Secondary Immunodeficiency Acquired diseases Medications Common Causes of Secondary Immunodeficiency Diseases/conditions Asplenia: particular concern with encapsulated organisms t Streptococcus pneumoniae, Haemophilus influenzae, and Neisseria meningitidis HIV shutsdownhelpertcellsmmmma.mg Cancers of the immune system Diabetes Mellitus Severe malnutrition Severe burns Medications Chemotherapy drugs cellshumoral deficiency Immunosuppressants Corticosteroids CD4 helper cellsare impaired slow down inflammation Clinical Manifestations of Infection Depends on body system affected Depends on extent Localized Superficial Deep Systemic fever shock Common symptoms Fever Pain Erythema Warmth Edema Identifying Infectious Agents Direct examination fast results Slide preparation of specimen and examination under a microscope May utilize stains Culture “Growing” microorganisms from a specimen Usually takes about 48 hours Aerobic vs anaerobic Able to perform susceptibility testing if order as culture and sensitivity antibiotic treatment to see if bug is susceptible to medicationsantibiotics Identifying Infectious Agents Antigen detection Do not require “growth” so can potentially provide more rapid results some Specific to an organism Nucleic acid detection (NAAT)PCRtesting Detect the genetic material (DNA or RNA) of a pathogen virus or bacteria Specific to an organism goodfor chlamydiagonorrhea Useful to detect organisms that are difficult to detect or slow growing Serology Detect antibodies titers booster shots Can detect present and past infections IgM: first antibody formed when encountering new pathogen 5 6 days recent More IgG: most abundant antibody, protects against future infections will persistaftermonths Gone 7 a ay Treatment of Infectious Diseases Observation Supportive care soup intubation vent Procedures I&D incisiona drainage Debridement Surgery Medications Antibacterials Antivirals Antifungals Antiparasitics Antibiotic MOA bacteriastatic Inhibitors of cell wall synthesis Inhibitors of folate synthesis Penicillins Sulfonamides preventbacteriafrom Cephalosporins multiplying WTErpositive Inhibitors of DNA replication Carbapenems Fluoroquinolones Glycopeptides Inhibitors of protein synthesis ***this is not an all inclusive list Aminoglycosides Tetracyclines Macrolides woffmornegative Lincosamides  Class Example MOA Coverage Examples of uses Penicillins Penicillin G Inhibit cell wall Gram + Strep, syphilis, Penicillin V synthesis anthrax Aminopenicillins Amoxicillin Inhibit cell wall Gram +/- ENT, respiratory, skin Ampicillin synthesis Anaerobes when infections Piperacillin combined with beta lactamase inhibitors ( clavulanate, tazobactum, sulbactum) Cephalosporins Inhibit cell wall ENT, respiratory, GU, synthesis skin infections 1st gen Cefazolin, cephalexin Gram + 2nd gen Cefuroxime, cefotetan Gram +, some Gram - 3rd gen Ceftriaxone, cefotaxime Gram – 4th gen Cefepime Gram – 5th gen Ceftaroline Gram +/-, MRSA, other resistant bugs EE Monobactams Aztreonam Inhibit cell wall synthesis Gram - Serious infections Carbapenems Imipenem Inhibit cell wall Gram +/-, anaerobes Serious infections, Meropenem synthesis intraabdominal Class Example MOA Coverage Examples of uses Glycopeptides Vancomycin Inhibit cell wall Gram + MRSA, c diff Tedmansyndromesynthesis Aminoglycosides Gentamicin Inhibit protein Gram - Bacteremia, Tobramycin synthesis abdominal infections Tetracyclines Tetracycline Inhibit protein Gram +/- Lyme disease, STIs, Doxycycline synthesis PID Macrolides Azithromycin Inhibit protein Gram +/- ENT, pneumonia, STIs Clarithromycin synthesis Lincosamides Clindamycin Inhibit protein Gram +, anaerobes Bacteremia, synthesis abdominal infections Sulfonamides Sulfamethoxazole Inhibit folate Gram +/- UTI, traveler’s Sulfadiazine synthesis diarrhea Fluoroquinolones Ciprofloxacin Inhibit DNA Gram +/- Respiratory and Levofloxacin replication urinary tract infections Antibio Gram 114111Mt The major sites of antiviral drug action. Note: interferon-α are speculated to have multiple sites of action on viral replication. (Reproduced with permission from Katzung BG, Vanderah TW: Basic & Clinical Pharmacology, 15th ed. New York, NY: McGraw Hill; 2021.) Citation: Chapter 49 Antiviral Agents, Katzung BG, Kruidering-Hall M, Tuan R, Vanderah TW, Trevor AJ. Katzung & Trevor's Pharmacology: Examination & Board Review, 13e; 2021. Available at: https://accessmedicine.mhmedical.com/content.aspx?sectionid=255307374&bookid=3058&Resultclick=2 Accessed: January 12, 2022 Copyright © 2022 McGraw-Hill Education. All rights reserved AccessMedicine > Sherris & Ryan's Medical Microbiology, 8e > Antiviral Agents and Resistance Kenneth J. Ryan Challenges in Infectious Disease Antimicrobial resistance Increasing number of resistant bugs MRSA VRE Vancomyosin resistant Presents a major threat to public health perscribing drugs spectrum Development of antimicrobial stewardship programs narrow Focused on minimizing toxicity and development of resistancepossibleftp.ffnce Reemerging diseases Human behavior anti vax Travel and commerce Antimicrobial resistance Breakdown of public health measures Methicillin-resistant Staphylococcus aureus (MRSA) Community acquired (CA-MRSA) Tends to cause skin and soft tissue infections Hospital acquired (HA-MRSA) Tends to cause invasive disease typically affects lungs Pneumonia, bacteremia, deep wound infections Colonization with MRSA Some institutions screen with nasal swab Place on contact precautions (gown and gloves) Decolonization can be considered Mupirocin intranasally twice daily Chlorhexidine baths orange prep before surgery  VRE Copyrights apply Vancomycin-resistant Enterococci (VRE) Common and difficult-to-treat cause of hospital-acquired infection Vast majority of VRE isolates are Enterococcus faecium Typically causes UTI, bacteremia, skin and soft tissue infections Risk factors are similar to that of MRSA Screening for colonization not common Contact precautions should be in place for patients with VRE No effective decolonization methods have been identified yet Bites and Rabies Nicole Scovazzo, EdD, PA-C Physician Assistant Studies PAS 521: Clinical Medicine I Lecture Objectives Describe the etiology of dog, cat and human bites Identify the common pathogens associated with dog, cat and human bites Describe the principles of bite management Distinguish when a bite should be managed with antibiotics Define rabies and describe its etiology Describe the incidence, clinical findings, diagnosis, treatment, prognosis and prevention of rabies Bites in the US 5-6 million animal bites occur annually in the US Most incidents are provoked and the animals are generally known by their victims Dog bites account for 80% of all animal bites Occur most commonly in the summer months Children are the highest risk for bites and serious injuries Cat and human bites are more likely to become infected that dog bites Cats bites 30-50% infection rate wounds Human bites 15-30% infection rate harder to cleantiny Dog bites 5% infection rate teethfpig.ge pfEd nhstkntes Eska Komnand bigger Human bites on the hand (fight bites) have a high risk of serious infection no subcutaneous tissue to protect onhand  has infectionlymphatics entered Lymphangitis. Severe lymphangitis extending from metacarpophalangeal wound up the arm from a “fight bite.” The red streak extends from the hand to the axilla, extending along lymphatic channels. (Photo contributor: Selim Suner, MD, MS.) Citation: 12-07 Lymphangitis, Knoop KJ, Stack LB, Storrow AB, Thurman R. The Atlas of Emergency Medicine, 5e; 2021. Available at: https://accessmedicine.mhmedical.com/content.aspx?bookid=2969&sectionid=250459398 Accessed: January 17, 2022 Copyright © 2022 McGraw-Hill Education. All rights reserved Common pathogens Biting species Common Pathogens Other considerations Dog Pasteurella multocida (50%) Consider rabies prophylaxis Strep Staph Capnocyytophaga canimorus Cat Pasteurella multocida (75%) Consider rabies prophylaxis bite Bartonella henselae (cat scratch disease)* Human, occlusional Viridans streptococci Staphylococcus aureus Haemophilus influenza anaerobes Human , clenched fist Eikenella corrodens fight bite Viridans streptococci Staphylococcus aureus Cat Scratch Disease Acute infection caused by Bartonella henselae Transmitted to humans via cat saliva (bites, licking, scratch) A few days after injury, a papule or ulcer may form at inoculation site. raised anddiscolored 1-3 weeks later fever, headache, malaise and regional lymphadenopathy develop Ifsa Disease is usually self-limited goes symptoms away on its own Immunocompromised individuals are at risk for disseminated infection spreads to other body systems w o elevation macule discoloration Principles of Bite Management History Examination Liberal cleansing Irrigation Closure/Culture Operative management Prophylactic antibiotics Tetanus immunization Elevation Rabies risk History What type of bite is it Provoked or unprovoked Location of animal PMH Medical conditions Allergies Immunizations of person and animal if known Examination Location of the bite increased infection Puncture wound or laceration Depth of the wound Any current signs of infection Evaluate underlying structures all fractures w bite are openfractures Liberal cleansing and Irrigation Wound must be cleansed very well 25% soap solution Eager Dilute povidone-iodine solution Copious irrigation with normal saline and a syringe  aerobic anaerobic Closure/Culture Culture every wound that appears infected Assess for need for closure Wounds at highest risk of infection, should not be closed if possible Cat or human bites Puncture wounds cosmeticpurposes t WE infectiontodrain out Hand or foot wounds Bites in immunocompromised patients anowspossible Signs of local infection upon first evaluation we Wounds > 12-24 hours Wounds that may be amenable to primary closure Dog bites Face or scalp wounds bleed alot cosmetic Simple, single layer wounds without devitalized tissue and no evidence of underling fracture Operative Management Tpp's Indications Foreign body factor's Necrotic tissue starter Joint involvement Fracture Consult ortho or general surgery Prophylactic antibiotics Prevention Indicated in all of the following: Cat bites All hand bites Immunocompromised patients Wounds in close proximity to bone or joint First line prophylaxis for all bites amoxicillin/clavulanate 875/125 mg BID x 5 days gram gram appears If wound infected already Initiate amoxicillin/clavulanate 875/125 mg BID x 5-14 days Tailor treatment based on culture results Infected hand bites require hospitalization with IV abx Cat Bite. Note the swelling and erythema to the index finger indicating infection, possibly with P multocida (a prominent and fastidious organism seen commonly with feline bites). (Photo contributor: Kevin J. Knoop, MD, MS.) Citation: 18-08 Animal Bite Wounds, Knoop KJ, Stack LB, Storrow AB, Thurman R. The Atlas of Emergency Medicine, 5e; 2021. Available at: https://accessmedicine.mhmedical.com/content.aspx?bookid=2969&sectionid=250461447 Accessed: January 17, 2022 Copyright © 2022 McGraw-Hill Education. All rights reserved Hand infection after a cat bite. Wound fluid culture grew Pasteurella multocida. [Photo contributed by J. S. Stapczynski, MD.] Citation: Chapter 46 Puncture Wounds and Bites, Tintinalli JE, Ma O, Yealy DM, Meckler GD, Stapczynski J, Cline DM, Thomas SH. Tintinalli's Emergency Medicine: A Comprehensive Study Guide, 9e; 2020. Available at: https://accessmedicine.mhmedical.com/content.aspx?bookid=2353&sectionid=218708499 Accessed: January 17, 2022 Copyright © 2022 McGraw-Hill Education. All rights reserved Tetanus immunization usually dog cat bites passive mm iafies e.in seat your antibodies get b ᵗh onlytime actively make its own antibodies our bodyhas to active immunity Elevation Minimize soft tissue swelling Rabies Risk Type of animal High-risk Low-risk domestic Availability of animal Observation Testing Rabies Rapidly progressive, zoonotic viral encephalitis Cause by infection with Rhabdoviridae Lyssavirus Rare in the US Usually due to wild animals Bats, raccoons, skunks, foxes Worldwide canine rabies is still prevalent 59,000 death annually  Rabies: Pathophysiology Virus crosses Invades Bite from NMJ and Virus binds Ascends the brain and Clinical signs infected enters and enters efferent spreads to and animal or air motor muscle cells nerves salivary symptoms droplets neurons and glands replicates Incubation period usually 3-7 weeks a  Rabies: Signs and Symptoms Prodromal phase: lasts about 10 days Pain, paresthesia or pruritus at site of infection Percussion myoedemaritening 85 Headache, fever and malaise Nausea and vomiting Abnormal sexual behavior aggressive Acute neurologic phase: lasts 2-7 days Encephalitic form: 80% of cases Delirium alternating with periods of calm Hypersalivation Hydrophobia Seizures Paralytic form: 20% of cases Acute ascending paralysis Coma and death unless treated Occurs rapidly once symptoms begin Usually from respiratory failure Rabies: Diagnosis Antemortem Direct fluorescent antibody testing on skin biopsy from nape of neck RT-PCR of CSF or saliva nucleic acid amplification test RNA DNA Serologic studies Serum antibodies Igmanto beelevated CSF Postmortem Look for Negri bodies in brain cells Eosinophilic inclusion bodies in cytoplasm of neurons  o Three large Negri bodies in the cytoplasm of a cerebellar Purkinje cell from an 8-year-old boy who died of rabies after being bitten by a rabid dog in Mexico. (From AC Jackson, E Lopez-Corella: N Engl J Med 335:568, 1996. © Massachusetts Medical Society.) Citation: Chapter 203 Rabies and Other Rhabdovirus Infections, Jameson J, Fauci AS, Kasper DL, Hauser SL, Longo DL, Loscalzo J. Harrison's Principles of Internal Medicine, 20e; 2018. Available at: https://accessmedicine.mhmedical.com/content.aspx?sectionid=192026000&bookid=2129&Resultclick=2 Accessed: January 17, 2022 Copyright © 2022 McGraw-Hill Education. All rights reserved Post-Exposure Treatment of Rabies Wound cleansing Post-exposure prophylaxis Determine the need on a case by case basis (see chart) Nearly 100% effective Prophylaxis with both active and passive immunity soon Once symptoms appear treatment is palliative and supportive Post-exposure treatment typically not effective any longer Death generally occurs within a week of symptom onset Rabies Postexposure Prophylaxis High risk wildlife: - Bat - Raccoon - Skunk - Fox - Coyote - Bobcat - Woodchuck Citation: Chapter 208 Rabies and Other Rhabdovirus Infections, Loscalzo J, Fauci A, Kasper D, Hauser S, Longo D, Jameson J. Harrison's Principles of Internal Medicine, 21e; 2022. Available at: https://accessmedicine.mhmedical.com/content.aspx?bookid=3095&sectionid=265434772 Accessed: December 28, 2022 Copyright © 2022 McGraw-Hill Education. All rights reserved  Rabies Prevention Vaccination of animals Rabies clinics Bait drop programs Vaccination should be given to high risk individuals Veterinarians Animal handlers Researchers who work with animals Travelers with lengthy stays in endemic countries doses on 2 booster previously immunized pts get day 0 and day 3 Do not need passive immunity  o ee ac ag Clostridial and Bacillus Infections Nicole Scovazzo, EdD, PA-C Physician Assistant Studies PAS 521: Clinical Medicine I Lecture Objectives Review the characteristics of the clostridial bacteria Differentiate between the following Clostridium species according to description, transmission, pathogenesis, sites of infection, diseases caused, signs and symptoms, and treatment: Clostridium tetani - tetanus Clostridium botulinum - botulism Clostridium perfringens – gas gangrene/myonecrosis Describe the transmission, pathogenesis, sites of infection, signs and symptoms and management of bacillus anthracis Clostridium species Anaerobic, spore-forming Gram-positive, rods Natural habitat is soil, sewage and the GI tract exotoxin Pathogenic Clostridia typically cause diseases that are toxin-mediated Clostridium tetani - tetanus Clostridium botulinum - botulism Clostridium perfringens – gas gangrene/myonecrosis Can also cause food poisoning Clostridium difficile – antibiotic associated diarrhea C diff Tetanus C. tetani is found in soil Spores are classically introduced via a puncture wound or abrasion where they proliferate and release toxin Rare disease in the developed world due to vaccination Tetanospasmin is the toxin responsible for the disease It interferes with neurotransmission at spinal synapses of inhibitory neurons by blocking GABA release primary inhibitory neurotransmitter spasm muscle Tetanus : Clinical Presentation Symptoms range from mild and local to disseminated and severe First symptom may be pain and tingling at site of inoculation with local muscle spasticity Other early signs of generalized tetanus are trismus (lock-jaw), muscle pain and stiffness, back pain, and difficulty swallowing As disease progresses muscle spasms become more severe and painful can cause crush injuries if severe Eventually disease progresses to involve airway and autonomic system SNS PNS Respiratory involvement can lead to asphyxia Involvement of autonomic system leads to cardiovascular events labilebloodpressure suddenspikein BPfromvasoconstriction Tetanus Diagnosis Differential diagnosis Meningitis Rabies Hypocalcemia Trismus due to peritonsillar abscess Diagnosis is clinical no testing necessary Tetanus: Management Goals of early treatment are to stop toxin production and neutralize circulating toxin Tetanus immune globulin (TIG) IM give ASAP Tetanus immunization Clean and debride wound Metronidazole IV q6h Supportive care to manage complications and control spasms Heavy sedation pts are veryexcitory Bed rest in a quiet, non-stimulating environment Mechanical ventilation Management of BP Tetanus Prevention Tetanus: Prognosis Mortality is low with treatment Recovery can take 4-6 weeks Mortality increased if delay in treatment wound is on head or face short incubation period early onset of seizures implies brain involvement Tetanus: Prevention fill strengthfor all 3 DTaP (for children under age 7) 5 dose series given at 2, 4, 6, 15-18 months, and 4-6 years Tdap Booster vaccine given at 11-12 years Full strength tetanus with smaller doses of diphtheria and pertussis Also given with each pregnancy Td (for adults > 19 years) Ttworyinariest Booster vaccine given every 10 years Full strength tetanus with smaller dose of diphtheria DTaPTdap strengths except forthose exposed to all the diseases regularly will getfull Botulism C. botulinum is found in the soil Botulinum toxin is highly potent and heat labile Seven types of neurotoxins A-G A is most severe Classified by CDC as high-priority agent due to potential use in bioterrorism  Types of Botulism Food-borne: caused by ingestion of pre-formed toxin in canned, smoked or vacuum packed foods About 20 cases annually in the US, most often caused by home-canned foods d Infant: caused by ingestion of bacteria containing honey in children 24 hours Risk Factors for Lyme Disease Residing in endemic areas Spending a lot of time in heavily wooded areas Recreational Occupational Lack of preventive measures Protective clothing Insect repellents Long duration of tick attachment Stages of Lyme Disease Stage 1: Early/localized infection Stage 2: Early disseminated infection Stage 3: Late, persistent infection Stage 4: Chronic Lyme Disease Stage 1: Early/Localized Infection Characterized by erythema migrans, “bulls-eye” lesion (red macule that expands to form an annular lesion with bright red border and central clearing) Rash develops about a week after tick bite Rash often accompanied by myalgias, arthralgias, headache and fatigue (“summer flu”) This stage typically resolves in 3-4 weeks even without treatment Stage 2: Early disseminated infection Occurs within days to weeks of the original infection Characterized by secondary annular skin lesions that are smaller Common symptoms include severe headache, mild neck pain/stiffness, fever, chills, migratory musculoskeletal pain, arthralgias, malaise and fatigue Neurologic deficits occur in 15% of patients Aseptic meningitis CN VII neuropathy resulting in facial palsy Cardiac manifestations occur in 8% of patients Most common is AV block Acute myopericarditis is possible Even if untreated symptoms are generally transient and resolve in a few weeks Stage 3: Late, Stage 4: Chronic Lyme persistent infection Disease Occurs months to years after Also known as post-Lyme initial infections syndrome Occurs in 60% of untreated Despite treatment patients patients continue to experience: Classic manifestation is mono- Pain or oligoarticular arthritis Neurocognitive issues involving large weight bearing fatigue joints, especially the knees Even if untreated, the arthritis is generally self-limiting Lyme Disease: Diagnosis Depends on presentation Clinical diagnosis if erythema migrans present Serology not recommended Atypical lesions and late disease Clinical manifestations Positive serologic studies Serologic tests for Lyme are not standardized Lyme Disease: Treatment Doxycycline 100 mg PO bid Length determined by stage of disease (10 days - 4 weeks) Alternate treatment Amoxicillin Cerfuroxime Azithromycin Coinfection with babesiosis and anaplasmosis should be considered if significant CBC abnormalities Prognosis is good Few patients develop residual side effects Lyme Disease: Prophylaxis Doxycycline 200 mg PO x 1 dose Indications Tick has been attached for at least 36 hours Prophylaxis can be started within 72 hours of tick removal More than 20% of ticks in the area are known to be infected with B burgdorferi No contraindication to doxycycline Rocky Mountain Spotted Fever (RMSF) Highest case-fatality rate of all rickettsial diseases Underrecognized by healthcare providers Nationally notifiable disease Causative agent R. rickettsia, transmitted by American dog tick Rocky Mountain wood tick Brown dog tick In the US estimated annual incidence is as high as 7 per 1,000,000 60% of cases occur in North Carolina, Oklahoma, Arkansas, Tennessee and Missouri  RMSF: Pathophysiology Bacteria Tick bites spreads via Increased Edema, human and blood and Tissue and vascular hypovolemia, feeds for at lymph and organ injury permeability ischemia least 6 hours infects epithelial cells RMSF Risk Factors Frequent exposure to woody or grassy areas Native American Men > women Age > 40 Severe illness more likely in: Children < 10 Those with G6PD deficiency Black males with G6PD deficiency at risk for fulminant RMSF Immunocompromised Delayed treatment RMSF Clinical Findings Classic triad of fever, rash and tick bite 2-14 days after inoculation symptoms begin with: High fever and chills Headache Nausea and vomiting Myalgias Restlessness and insomnia Irritability 2-6 days after fever, characteristic rash shows up Faint macules that progress to maculopapules and then petechiae Rash initiates on wrists and ankles and spreads centrally up the extremities to the trunk Palms and soles are characteristically affected Diagnosing RMSF Labs not specific but commonly demonstrate Thrombocytopenia Hyponatremia Elevated ALT and AST Hyperbilirubinemia Serology usually becomes positive 7-10 days after onset, important to use paired sera Skin biopsy of lesions reveals vasculitis with distinctive, unique perivascular lymphocytic infiltrate Treatment and Complications of RMSF Doxycycline 100 mg PO or IV BID continue 3-5 days after defervescence If doxy contraindicated then treat with chloramphenicol Patient may develop multiple other sequelae as a result of organ injury that also require treatment and admission: Lungs: Cough, pneumonitis, ARDS CNS: Delirium, stupor, seizures or coma GI: Hepatomegaly and jaundice Renal: Uremia Mortality rate of 3-5% among treated patients Untreated patients usually die within 2 weeks Babesiosis Caused by the protozoa Babesia Transmitted to human by Ixodes tick bite In the US most cases occur in the Northeast during summer Mild flu-like illness may occur but many infections are asymptomatic and do not require treatment Severe illness likely to occur in those who are immunosuppressed Identification of intraerythrocytic parasite on peripheral blood smear with PCR testing for diagnosis Treatment: atovaquone + azithromycin or quinine + clindamycin Ehrlichiosis and Anaplasmosis Causative agents Ehrlichia chaffeensis Transmitted via Lone Star tick Anaplasma phagocytophilum Transmitted via Ixodes tick Patients present with flu-like illness of fever, myalgia, headache and malaise Disease can be severe in both cases, however in ehrlichiosis up to 77% of patients require hospitalization and can be fatal in 2% Diagnosis with PCR or serology Treatment for both is doxycycline Prevention of Tick-borne Illnesses Avoid tick-infested and heavily wooded areas Wear protective clothing Utilize tick and insect repellents “Tick checks” with prompt removal if found A 14-year-old boy is brought in due to a tick bite. He arrived at summer camp in Vermont earlier today and spent the afternoon outdoors. About an hour ago, the patient noticed a tick attached to his right thigh. He has no fever or pain at the site. Vital signs are normal. Physical examination shows a small, brown tick attached to the right medial thigh with a small area of erythema. The remainder of the examination is unremarkable. Which of the following is the best next step in management of this patient? A. Allow the tick to detach spontaneously and obtain Lyme disease serology B. Apply petroleum jelly and prescribe doxycycline for 21 days C. Crush the tick and prescribe single-dose doxycycline D. Puncture the body of the tick and prescribe amoxicillin for 21 days E. Remove the tick with small forceps and reassure the patient  4 12daysroughly sex until infection is gone Nothaving  alert public health department ontoo much no longerreport risk complications gram diplococci test for both men eyes becomeinfected from vaginal birth so No one  BID resistance have to come back in 4 6 weeks for re check  then goes for  Asymptomatic screening available found in the oropharangeal Nff So contraindicated pregnancy m  more common in men whohavesexwmen diagnosed by egomanommandfferentiistimammanbloodworker becomes.tt inMate In treatment is the same Always a board Q  Blood screening menwhohavesex with men  _Fedft Synonymous with syphilis Rash including palmsasoles look like wartygrowths Check for herpestoo Secondary Syphilis NOT genital wart aofft prostitutepupil or Syphilis if they're born  tests Multiple blood inina we not of  to there 17 Antreat injection  experiment Syphilis  1 STD more common severein women  boarders irregular Clinical Dx cause can headthers  lice pubic scratches sexual abuse worriedmost freanattower Fungal Diseases Physician Assistant Studies PAS 521: Clinical Medicine I 2025 Lecture Objectives Describe the classification of fungi Describe Pityriasis versicolor in terms of causative agent, location of infection, clinical presentation, and diagnosis Compare and contrast the dermatophytoses in terms of location of infection, clinical presentation, diagnosis and treatment Describe histoplasmosis in terms of causative agent, location of infection, clinical presentation, and diagnosis Compare and contrast the opportunistic mycoses in terms of causative agent, location of infection, clinical presentation, diagnosis and treatment Overview of Fungal Disease Fungi can grow in two forms Molds (hyphae) Yeasts (budding) May appear as pseudohyphae Grow in warm, moist environments Part of normal microbiota Categorization of Fungi Superficial Cutaneous Subcutaneous Systemic Opportunistic  Fungal Diseases *not all inclusive Superficial Cutaneous Systemic Opportunistic take advantageof immunoincompetent Pityriasis versicolor Dermatophytoses Histoplasmosis Candidiasis Coccidioidomycosis Cryptococcus Blastomycosis Pneumocystis Pityriasis Versicolor (Tinea Versicolor)Superficial Caused by the yeast Malassezia Lesions consist of oval scaly, macules, papules and patches concentrated on the trunk Hyperpigmented on light skin Hypopigmented on dark skin Often patients will complain of spots that will not tan Typically not pruritic Diagnosed with KOH prep of skin scrapings “spaghetti and meatballs” (short hyphae and round spores) Treatment with topical selenium sulfide, topical antifungals or oral Fluconazole selsin blue shampoo Citation: Chapter 141 Fungal Overview, Usatine RP, Smith MA, Mayeaux, Jr. EJ, Chumley HS. The Color Atlas and Synopsis of Family Medicine, 3e; 2019. Available at: https://accessmedicine.mhmedical.com/content.aspx?bookid=2547&sectionid=206791980 Accessed: January 18, 2022 Copyright © 2022 McGraw-Hill Education. All rights reserved Dermatophytoses Also called tinea or ringworm Tame Caused by dermatophytes Trichophyton Epidermophyton Microsporum Typically spread from human to human by direct contact Named for the location affected Dermatophytoses by Location Tinea corporis: body ring worm Tinea capitis: head Most common dermatophytosis in children Tintinalli's Emergency Medicine: A Comprehensive Study Guide, 9e > Rashes in Infants and Children Judith E. Tintinalli, O. John Ma, Donald M. Yealy, Garth D. Meckler, J. Stephan Stapczynski, David M. Cline, Stephen H. Thomas Subcutaneous Mycoses Usually caused by environmental fungi that enter subcutaneous tissue by traumatic inoculation digging Typically cause lesions that become granulomatous and expand slowly from site of inoculation May become systemic, and life-threatening, in rare cases Generally treated with oral antifungals Surgical debridement may be necessary Systemic Mycoses Inhalation of fungus leads to pulmonary infection Majority are asymptomatic or self-limiting Immunocompromised at risk for disseminated disease which is often fatal Examples Histoplasmosis Coccidioidomycosis Blastomycosis Paracoccidioidomycosis Histoplasmosis Biggest risk factor is exposure to bird and bat droppings Most often asymptomatic If symptomatic usually mild-flu like illness Diagnosis with antigen testing Imaging is nonspecific Treatment indicated for progressively symptomatic patients and immunocompromised Oral itraconazole antifungal Poor prognosis for those with disseminated disease Coccidioidomycosis “Valley Fever” Found in arid regions of southwestern US, Mexico and Central/South America 40% of primary infections are symptomatic Flu-like illness, erythema nodosum is common Opportunistic infection in AIDS patients in endemic areas Diagnosis is via serology Imaging varies dependent upon extent of disease Treatment Oral itraconazole or fluconazole May need surgical debridement for abscesses or necrosis Blastomycosis Endemic in south, central and midwestern US and Canada Usually occurs in immunocompetent individuals secondary to outdoor occupational or recreational activities May be asymptomatic Cough, moderate fever, dyspnea, and chest pain common if symptomatic Wart like Raised, verrucous cutaneous lesions are commonly present in disseminated disease Chest imaging usually reveals lobar consolidation Diagnosis is via antigen testing Treatment with oral itraconazole  covered usually 1 spores creates Eves portM my Opportunistic Mycoses Disseminated infection caused by fungi that are Normal flora Environmental May be rapidly progressive and fatal Prophylaxis is indicated in certain populations Leukemia Transplant patients AIDS “Take advantage” of host immunosupression Candidiasis Caused by Candida albicans Normal flora Disease occurs when Disruption of other normal flora Immunodeficiency Types of disease caused byantibiotics Mucocutaneous Invasive Persistent mucocutaneous candidiasis should raise suspicion ??Underlying condition?? probably mimunosuppressed Cutaneous Candidiasis (Intertrigo) diaper rash Hot and humid climates predisposes Obesity Clinical presentation Intensely pruritic, beefy-red areas in body folds with maceration or fissuring Satellite papules and pustules common Clinical diagnosis foul odor Management Preventive measures Localized antifungal topical Topical –azole +/- hydrocortisone cream Widespread maybemixedin notusedalone Fluconazole po Candidiasis: diaper dermatitis Confluent erosions, marginal scaling, and "satellite pustules" in the area covered by a diaper in an infant. Atopic dermatitis or psoriasis also occurs in this distribution and may be concurrent. Citation: SECTION 26 FUNGAL INFECTIONS OF THE SKIN, HAIR, AND NAILS, Wolff K, Johnson R, Saavedra AP, Roh EK. Fitzpatrick's Color Atlas and Synopsis of Clinical Dermatology, 8e; 2017. Available at: https://accessmedicine.mhmedical.com/content.aspx?bookid=2043&sectionid=154894494 Accessed: January 21, 2022 Copyright © 2022 McGraw-Hill Education. All rights reserved Cutaneous candidiasis: intertrigo Small peripheral "satellite" papules and pustules that have become confluent centrally, creating a large eroded area in the submammary region. Citation: SECTION 26 FUNGAL INFECTIONS OF THE SKIN, HAIR, AND NAILS, Wolff K, Johnson R, Saavedra AP, Roh EK. Fitzpatrick's Color Atlas and Synopsis of Clinical Dermatology, 8e; 2017. Available at: https://accessmedicine.mhmedical.com/content.aspx?bookid=2043&sectionid=154894494 Accessed: January 21, 2022 Copyright © 2022 McGraw-Hill Education. All rights reserved Oral Candidiasis (Thrush) Risk factors Immunodeficiency Denture use Xerostomia mouth Antibiotics dry Inhaled corticosteroids asthmaCOPD May be first manifestation of HIV Oral Candidiasis: Presentation and Management Clinical presentation Erythema of tongue or oral mucosa with curd-like white patches Accompanying discomfort PATCHES WILL SCRAPE OFF Clinical diagnosis Management Preventative measures Topical antifungals (clotrimazole, miconazole or nystatin) Oral antifungals (fluconazole) Oral candidiasis: thrush Extensive cottage cheese-like plaques, colonies of Candida that can be removed by rubbing with gauze (pseudomembranous), on the palate and uvula of an individual with advanced HIV/AIDS. Patches of erythema between the white plaques represent erythematous (atrophic) candidiasis. Involvement may extend into the esophagus and become associated with dysphagia. Citation: SECTION 26 FUNGAL INFECTIONS OF THE SKIN, HAIR, AND NAILS, Wolff K, Johnson R, Saavedra AP, Roh EK. Fitzpatrick's Color Atlas and Synopsis of Clinical Dermatology, 8e; 2017. Available at: https://accessmedicine.mhmedical.com/content.aspx?bookid=2043&sectionid=154894494 Accessed: January 21, 2022 Copyright © 2022 McGraw-Hill Education. All rights reserved Vulvovaginal Candidiasis One of the most common causes of vaginitis Not sexually transmitted Risk factors DM Antibiotic use Pregnancy estrogen Immunosuppression Genetic predisposition Poor hygiene practices Wearing clothes that do not breathe Post Menopause Wet clothing vaginalpHchanges Vulvovaginal Candidiasis Clinical presentation Vulvovaginal itching Thick, adherent, curd-like white discharge that has no odor Clinical diagnosis KOH wet mount shows hyphae Joneses Management intravaginal Preventive measures Vaginal antifungals (topical -azoles) Widely available OTC Oral antifungals (fluconazole) Esophageal Candidiasis Occurs most commonly in those with significant immunosuppressionAIDS Clinical presentation Substernal odynophagia payflowing GERD Nausea +/- oral candidiasis Diagnosed with endoscopy and brushings Management PO or IV fluconazole Candida esophagitis. Note the many whitish lesions on the esophageal mucosa seen on endoscopy. (Reproduced with permission from McKean SC, Ross JJ, Dressler DD, et al: Principles and Practice of Hospital Medicine. New York, NY: McGraw Hill; 2012.) Citation: Chapter 73 Gastrointestinal Tract Infections, Levinson W, Chin-Hong P, Joyce EA, Nussbaum J, Schwartz B. Review of Medical Microbiology & Immunology: A Guide to Clinical Infectious Diseases, 17e; 2022. Available at: https://accessmedicine.mhmedical.com/content.aspx?bookid=3123&sectionid=262002510 Accessed: January 21, 2022 Copyright © 2022 McGraw-Hill Education. All rights reserved Invasive Candidiasis Candidemia or deep-seated infection without candidemia Risk highest among critically ill patients and those with intravascular catheters Especially if TPN being administered liquidnutrition Wide range of presentations from mild fever to septic shock Diagnosed with blood cultures May be normal in 50% of cases Management Remove all lines and send tip for culture IV echinocandins (newer class of antifungals) Capsofungin, micafungin, anidulafungin Cryptococcal Meningitis Bad Caused by Cryptococcus neoformans usual Most common cause of fungal meningitis Seen in immunocompromised individuals Clinical presentation Headache and altered mental status Diagnosed with serum or CSF antigen testing (CRAG) No LP is diagnostic procedure of choice shakeandbake Induction therapy with Amphotericin B IV and flucytosine PO Maintenance antifungal therapy with fluconazole PO Pneumocystis Pneumonia PSP PCP Caused by Pneumocystis jirovecii Occurs in up to 80% of AIDS patients not receiving prophylaxis Clinical presentation Subacute onset of nonproductive cough and DOE dyspnea on exertion Findings usually disproportionate to degree of illness Diagnosis with CXR CXR may be normal or show diffuse interstitial disease PCR testing of sputum, bronchoalveolar lavage fluid or lung tissue DOC is trimethoprim-sulfamethoxazole (Bactrim) PO Prednisone may be adjuvant therapy in severe cases Prophylaxis is indicated once CD4 count is 50 years ago Remains endemic in the tropics Morbidity and mortality greatest in Africa a Responsible for 1200 deaths daily worldwide Most deaths occur in young children Undeveloped antimalarial immunity o oo Severe disease is also likely in travelers due to lack of developed immunity Clinical Presentation of Malaria Symptomatic malaria is only caused by the erythrocytic stage Symptoms consist of flu-like illness followed by malarial paroxysm of chills, high fever, then sweats Signs may include anemia, hepatosplenomegaly, jaundice Severe malaria (Falciparum malaria) is a medical emergency Parasitemia level > 5% Characterized by signs of organ failure Severe anemia Coagulopathy Altered mental status Seizures Acute kidney injury ARDS Circulatory shock Diagnosis of Malaria Gold standard diagnostic test is Giemsa-stained blood smears If smear is negative and suspicion for disease is still high repeat every 8-24 hours x 3 to rule out malaria CBC shows mild-severe anemia CMP reveals elevated LFTs and hyperbilirubinemia If severe disease is present labs will reveal appropriate findings Thin film Giemsa-stained micrograph with Plasmodium falciparum ring forms. (From Steven Glenn, Laboratory & Consultation Division, Public Health Image Library, CDC.) Citation: 37-04 Malaria, Papadakis MA, McPhee SJ, Rabow MW, McQuaid KR, Gandhi M. Current Medical Diagnosis & Treatment 2024; 2024. Available at: https://accessmedicine.mhmedical.com/content.aspx?bookid=3343&sectionid=279780547 Accessed: January 15, 2024 Copyright © 2024 McGraw-Hill Education. All rights reserved Treatment of Malaria First line treatment for malaria was chloroquine, however resistance is becoming an issue (especially for P. falciparum) Drug regimens are based on species, resistance testing and severity of infections Even those with uncomplicated falciparum malaria should be admitted in the US due to risk of rapid progression to severe disease Other supportive treatments as necessary Prevention of Malaria Chemoprophylaxis for all travelers from nonendemic region to endemic region Regimen recommendations from the CDC Use of bed nets, especially those treated with permethrin insecticides Mosquitoes are most active at dawn and dusk Use of insect repellents and insecticides Vaccines becoming available Use parasitic antigen 25-75% efficacy depending on type Toxoplasmosis Caused by the protozoa Toxoplasma gondii Found worldwide Definitive hosts are cats Transmission to humans occurs via: Ingestion of cysts in raw or undercooked meat Ingestion of oocysts in food or water contaminated by cats Transplacental transmission pregnant women should not cleanthe litter box Incidence of 1.1 million persons each year in the US Four Presentations of Toxoplasmosis 1. Primary infection in the immunocompetent person healthy Infection established in the GI tract and the travels to the lymphatics and disseminates 10-20% asymptomatic Acute infections are mild and resemble infectious mononucleosis 2. Congenital infection Fetal infection occurs in 30-50% of cases when a nonimmune mom becomes infected Risk of transmission increases by trimester Severity of illness worse the earlier infection occurs Stillbirths, severe neonatal disease with early infection Late infection often results in subtle abnormalities and progresses to symptoms later in life Four Presentations of Toxoplasmosis 3. Retinochoroiditis Most common late presentation of congenital toxoplasmosis Occurs weeks to years after infection Presents as pain, photophobia, visual changes and may progress to glaucoma and blindness 4. Disease in the immunocompromised person Most common presentation is encephalitis with multiple necrotizing brain lesions Presents subacutely with fever., altered mental status, focal neuro deficits Can also cause chorioretinitis, pneumonitis or myocarditis Diagnosis of Toxoplasmosis Serologic testing performed most commonly Not part of routine screening among pregnant women in the US Ideally they should be screened and those at high risk should be screened multiple times during pregnancy In immunocompromised individuals imaging of the brain reveals multiple ring enhancing cerebral lesions Treatment and prevention Treatment generally not indicated in immunocompetent, non-pregnant individuals Acute infection in pregnancy Spiramycin Standard therapy in other patients Pyrimethamine + sulfadiazine + folinic acid PREGNANT MOMS DO NOT CHANGE/CLEAN THE LITTERBOX! Prevention of Toxoplasmosis Avoidance of undercooked meat Avoidance of contact with material contaminated with cat feces Wear gloves when gardening Chemoprophylaxis with TMP-SMX (Bactrim) in certain populations AIDS Transplant recipients Helminths: Overview Parasitic worms 3 groups Nematodes (roundworms) Cestodes (tapeworms) Trematodes (flukes) Most infections are acquired by ingestion of eggs or larvae Other means of infection are larvae penetration of skin or vector-borne Worms inhabiting the intestine are easier to treat vs those inhabiting tissues Anthelmintic drugs kill or stun parasitic worms, causing them to be expelled from the body Enterobius (Pinworm)verycommon in children Affects about 40 million people in the US Primarily children Gravid female worms migrate from the cecum to perianal region where they release eggs that become infective Person-to-person spread occurs from perianal scratching and transport of infective eggs to mouth Presents as perianal itching that is worst at night extreme Diagnosed by microscopy of tape applied to perianal region in AM Treatment with mebendazole or albendazole (anthelmintic drug) Household members should be treated also Pinworms. Multiple tiny pearly white worms are seen at the anus. (Photo contributor: Lawrence E. Heiskell, MD.) Citation: 14-44 Pinworm Infection (Enterobiasis), Knoop KJ, Stack LB, Storrow AB, Thurman R. The Atlas of Emergency Medicine, 5e; 2021. Available at: https://accessmedicine.mhmedical.com/content.aspx?bookid=2969&sectionid=250460551 Accessed: January 19, 2022 Copyright © 2022 McGraw-Hill Education. All rights reserved  Ascariasis Most common intestinal helminth Prevalent in areas of poor sanitation Infections occurs secondary to ingestion of eggs in contaminated food or water Pigs Most infections asymptomatic unless high worm load Abd tenderness Migration may cause emesis of worms or biliary and pancreatic disease Very heavy infection may lead to bowel obstruction Diagnosis based on visualization of worms Stool analysis All infections should be treated with albendazole or mebendazole Hookworm Common in tropical and subtropical regions Larvae found in moist soil Penetrate skin and migrate to pulmonary capillaries and eventually GI tract Once attached to intestinal mucosa they suck blood Manifestations Transient pruritic rash and cough/wheezing with low-grade fever Abd pain, anorexia, diarrhea Anemia Diagnosis made by demonstration of eggs in stool Stool may also have occult blood Treatment with albendazole or mebendazole  Nematodes = Roundworms Trichinella (Trichinosis) Infection results when pork that contains larvae is consumed Annual incidence of 12 cases in the US undercooked pork Larvae invade small bowel where they mature and release new larvae that migrate to striated muscle Number of larvae per gram of muscle dictates severity of disease Often asymptomatic If symptomatic Week 1: GI upset Following weeks: progressive fever, myalgias, periorbital edema Trichinella (Trichinosis) Diagnosis Serology Muscle biopsy worstcase scenario Early on pharmacotherapy may help prevent progression of disease Mebendazole or albendazole No specific treatment for systemic disease Supportive care only Prevention Cook pork thoroughly using thermometer Cestodes (Tapeworms): Overview Intestinal infections are generally asymptomatic Except for visible worms in stool Symptoms may develop related to cysts and/or cyst rupture Brain Liver Lung Treatment of choice is typically single dose of praziquantel (anthelmintic drug)  Parasitic blood fluke Schistosomiasis Infects 230 million people worldwide >70% of cases occur in sub-Saharan Africa Most often worm penetrates human skin or mucous membranes after exposure via fresh body of water (lakes, ponds, rivers) in endemic area the flukes are found in snails and then are shed into the water. Schistosomiasis Clinical manifestations Cercarial dermatitis: pruritic rash for 1-2 weeks (swimmers rash) supportive only Acute schistosomiasis: constitutional symptoms, abd tenderness, transient pulmonary infiltrates Chronic schistosomiasis Intestinal: microulcerations and superficial bleeding Urogenital: dysuria that progresses over years to urinary retention and incontinence Pulmonary: pulmonary hypertension CNS: seizures, encephalopathy Need stool culture Diagnosis of acute/chronic: by history and presence of eggs in excreta Treatment of choice is typically single dose of praziquantel YUCK!! HIV/AIDS Nicole Scovazzo, EdD, PA-C Physician Assistant Studies PAS 521: Clinical Medicine I Lecture Objectives 1. Differentiate between HIV and AIDS 2. Describe the transmission and pathogenesis of HIV 3. Describe the epidemiology and risk factors associated with HIV/AIDS 4. Differentiate between the different stages of HIV infection/AIDS and the immune response at each of those stages 5. Describe the methods used to diagnose HIV/AIDS 6. List the most common opportunistic infections that occur in HIV/AIDS patients and when chemoprophylaxis against the infections should be initiated 7. Describe the function of anti-retroviral treatment in HIV infection and the current 1st line agents 8. Formulate an approach to educating patients on HIV transmission and dispelling ,myths and fears concerning HIV and AIDS 9. Differentiate between pre- and postexposure prophylaxis and identify current preferred drug regimens 10. Describe the prognosis associated with HIV infection Definitions HIV +: positive HIV serology AIDS: multiple definitions per the CDC Presence of opportunistic infections and malignancies that rarely occur in the absence of severe immunodeficiency Positive HIV serology and certain infections and malignancies that can occur in immunocompetent hosts but are more common among persons infected with HIV Positive HIV serology and nonspecific conditions, such as dementia and wasting Individuals with positive HIV serology who have ever had a CD4 lymphocyte count below 200 cells/mcL or a CD4 lymphocyte count below 14% CDC AIDS case definition diagnoses: https://accessmedicine.mhmedical.com/ViewLarge.aspx?figid=288497554 &gbosContainerID=0&gbosid=0&groupID=0&sectionId=288497545 Etiology Caused by infection with the human retroviruses HIV-1 or HIV-2 HIV-1 is most common cause of AIDS worldwide RNA retrovirus Viruses are transmitted through: Sexual contact Sharing of contaminated needles and/or syringes among injection drug users viral load morelikely to transmit Intrapartum or perinatally Breast milk Transfusion of blood or blood products HIV is NOT transmitted through: Insect bites Saliva, tears or sweat Hugging, shaking hands, sharing toilets, sharing dishes The air  integrates into hostDNA made vival DNA Citation: Chapter 197 Human Immunodeficiency Virus Disease: AIDS and Related Disorders, Jameson J, Fauci AS, Kasper DL, Hauser SL, Longo DL, Loscalzo J. Harrison's Principles of Internal Medicine, 20e; 2018. Available at: https://accessmedicine.mhmedical.com/content.aspx?bookid=2129&sectionid=192025263 Accessed: January 04, 2021 Copyright © 2021 McGraw-Hill Education. All rights reserved  lymphoid tissue viremia lymphnodes t tnout Events that transpire from primary HIV infection through the establishment of chronic persistent infection to the ultimate destruction of the immune system. See text for details. CTLs, cytolytic T lymphocytes; GALT, gut-associated lymphoid tissue. Citation: Chapter 197 Human Immunodeficiency Virus Disease: AIDS and Related Disorders, Jameson J, Fauci AS, Kasper DL, Hauser SL, Longo DL, Loscalzo J. Harrison's Principles of Internal Medicine, 20e; 2018. Available at: https://accessmedicine.mhmedical.com/content.aspx?bookid=2129&sectionid=192025263 Accessed: January 04, 2021 Copyright © 2021 McGraw-Hill Education. All rights reserved Epidemiology Worldwide, at the end of 2022 Prevalence of 39 million adult cases Incidence of 1.33 million adult cases United States, at the end of 2021 Estimated prevalence of 1.2 million adults and adolescents Incidence of roughly 36,000 cases Certain populations disproportionately affected MSM Transgender persons Racial/ethnic disparities Risk Factors Sexual transmission Unprotected sex, especially with multiple partners Higher risk with male-to-male sexual contact Having another STD Circumcised males 65% less likely to acquire HIV through heterosexual intercourse Don't trap secretions Transmission through blood or blood products Injection drug use Unsterile piercing, tattoos Occupational  tears morelikelyto cause Copyrights apply Stages of HIV Infection/AIDS Primary Infection Some patients have no symptoms 50-70% develop “acute retroviral syndrome” Occurs 3-6 weeks following infection Symptoms similar to mononucleosis constitutional symptoms malaisegeneral unwell Establishment of persistent and chronic infection Period of clinical latency No signs symptomsDetermined by viral load Median time is estimated to be 10 years During this phase, without antiretroviral therapy, the virus continues to replicate and CD4+ cell counts fall Advanced HIV disease Wide spectrum of opportunistic complications are associated with advanced HIV disease As CD4+ count levels drop to