Bacterial and Atypical Infections - Lecture Notes PDF

Bacterial & Atypical Infections Matthew J. Kesic, PhD, PA-C  Bacterial & Atypical Infections “Instructional Objectives” At the conclusion of this lecture and completion of required readings, th...

Bacterial & Atypical Infections Matthew J. Kesic, PhD, PA-C  Bacterial & Atypical Infections “Instructional Objectives” At the conclusion of this lecture and completion of required readings, the student will be able to: 1. Discuss the medically important bacteria that are of importance in the US population by describing the pathophysiology and clinical syndromes associated with each organism. 2. Explain how gram stain characteristics are related to bacterial structure. 3. Describe the basis for the Lancefield groups for Streptococci. 4. Name the common human normal flora by anatomic location. 5. Define an “opportunistic pathogen”. 6. Recognize and explain the following terms related to infection: invasion, colonization, carrier, virulence. 7. Contrast the disease-causing mechanisms of endotoxin and exotoxin. 8. Define aerobe, anaerobe, and facultative anaerobe. 9. Summarize the medically important viruses that are of importance in the US population by describing the portal of entry and pathophysiology of each agent. Describe the laboratory techniques used to diagnose each of the clinically important viruses. Describe the clinical syndromes associated with each virus. 10. Discuss the pathogenesis and spectrum of disease in HIV infection through the range of CD4 counts. Text: Current Medical Diagnosis & Treatment  Bacterial & Atypical Infections “Instructional Objectives” At the conclusion of this lecture and completion of required readings, the student will be able to: 1. List the important perinatal viruses (and other TORCH infections) and their modes of transmission. Describe the clinical syndromes with which each is associated. 2. List the clinically important viruses that have an animal reservoir. Describe the modes of transmission and the diseases with which they are associated. 3. Explain the ways in which individuals can have persistent viral infections. 4. Discuss the most likely causes of sepsis based on the knowledge of the initial site and sources of infection. 5. List the most common causes of adult vs. pediatric sepsis. 6. Explain factors that increase the risk for sepsis. 7. Describe the sequence of events that lead to septic shock (e.g., microbial triggers and host mediators). 8. Describe the differences among the following: sepsis, severe sepsis, septic shock, and multiple organ dysfunction syndrome (MODS) and sequential organ failure assessment score (SOFA). 9. Evaluate clinical scenarios regarding sepsis. a. Describe the clinical use of procalcitonin. 10. What are the primary risk factors for infection with Entamoeba, Giardia, and Cryptosporidium. Describe the diagnostic criteria and clinical presentation of each. 11. Describe the method of diagnosis and clinical presentation of infection with Trichomonas vaginalis. 12. Describe the risk factors and clinical presentation of malaria. 13. Name the primary helminthic infestations of concern in the US. Name the risk factors associated with each (including geography). 14. Describe the diagnostic criteria and clinical presentation for infestation with Enterobius. 15. Describe the role of immunosuppression in systemic fungal infection. 16. List the body’s normal defenses against mycotic infection. 17. Describe the clinical and laboratory methods used to diagnose specific fungal infections. 18. Name the common organisms and clinical manifestations associated with dermatophyte infection. 19. Describe the clinical presentation of tinea versicolor. 20. Name the primary risk factor for sporotrichosis and describe its clinical presentation. 21. Describe the common clinical syndromes associated with Candida infection. Name the primary risk factors for each. 22. Describe the risk factors and clinical presentation for Coccidioidomycosis, Histoplasmosis and Blastomycosis.  "Gram Stain" Gram - Positive/Negative Term used by microbiologist to classify bacteria into two groups  Gram – Positive  Gram- Negative Han Christian Gram (1884)……… This stain will either stain the cells: Purple (Positive) Red/Pink (Negative) Positive/Negative reference is based on bacterium’s chemical and physical cell wall properties Gram Stain Test Bacteria are dyed with crystal violet (purple) Bacteria are washed with decoloring solution Counterstain is added: Safranin or fuchsine Bacteria are washed again…….  Gram-Positive bacteria retain their crystal violet dye  Gram-Negative bacteria are stained red/pink  GRAM POSITIVE Gram-Positive bacteria have a very thick cell wall made of a protein called peptidoglycan Bacteria retain the crystal violet dye Gram-Positive bacteria Do NOT have an outer cell membrane found in Gram- negative bacteria  GRAM NEGATIVE Gram-Negative bacteria have a very thin peptidoglycan layer that is sandwiched between Inner cell membrane Bacterial outer membrane Gram-Negative bacteria Do NOT retain the crystal violet stain Decolorized to accept counter stain (Safranin or Fuchsine) Stain pink……..thus why they are called gram-negative  Gram Positive Bacterial Infections Lancefield Grouping: Classification system for streptococci Developed by Rebecca Lancefield in the 1930s Designated by letters (A, B, C, etc.)  Staphlococcus Aureus “Gram Positive” Staph aureus “S. aureus” Gram positive bacteria in grape-like clusters ~ 25% of patients are ASYMPTOMATIC carriers Why are they infected? Skin & Nasal carriage Decreased immune system Cutaneous barrier is broken (cuts, cracks) Types of infection:  Skin infections  Impetigo  Abscesses Exfoliative Toxin TSST-1 Food poisoning Acute endocarditis Pneumonia Osteomyelitis cdc.gov  Staphlococcus Aureus “Gram Positive” Diagnosis Wound culture (positive) Blood culture (positive) Definitive treatment: Incision and drainage (I&D) Wound Care Antibiotics MSSA - Methicillin Sensitive Staph Aureus Penicillin 1st generation Cephalosporins (Keflex) MRSA - Methicillin Resistant Staph Aureus “Alters the penicillin binding proteins (PBP)” Bactrim (Sulfonamides) Doxycycline (Tetracycline) Clindamycin Vancomysin Linezolid  Staph Aureus Osteomyelitis “Gram Positive” Infection involving bone ~ 60% of bone infections are related to Staph Aureus Etiology/Classification: Nonhematogenous Direct inoculation (bone fracture or joint replacement) Spread from surrounding soft tissue Hematogenous Infection that seed the bone in the setting of bacteremia  Signs and Symptoms of Osteomyelitis “Gram Positive” Clinical presentation:  Signs of infection Pain Localized tenderness Warmth/erythema Fever Malaise Diaphoresis Bone pain is also a symptom DM II (may not have pain)  Staph Bacteremia “Gram Positive” Presence of viable bacteria in the circulating blood  Diagnosis from Blood Cultures (POSITIVE) Possible etiology/complications….. 1. Endocarditis 2. Osteomyelitis 3. Implantable device or hardware from surgery Treatment : ❑ If skin is the source…..  10-14 days of antibiotic therapy ❑ All others…….  4-6 weeks of IV antibiotic therapy  Removal of hardware when patient stabilizes  Toxic Shock Syndrome Toxin (TSST-1) “Gram Positive” Life-threatening complication of certain types of bacterial infections Results from toxins Super T-cell antigens Super T-cell Antigens: Massive T-cell Activation: Produced by 5 to 25% of Staphylococcus aureus isolates Superantigens can activate up to 20% of the body's T- TSST-1 binds to the T-cell receptor and MHC class II molecules cells, compared to the Induce expansion of both CD4+ and CD8+ subsets of T Lymphocytes typical 0.01% activated by conventional antigens. Release of large amounts of interleukin-1, interleukin-2 and tumor necrosis factor “Staphylococcal and streptococcal toxic shock syndrome toxins (TSST-1, streptococcal pyrogenic exotoxins, streptococcal mitogenic exotoxin Z) are superantigens that can activate large numbers of circulating T cells to release cytokines.” Produced by Staphylococcus aureus (staph) bacteria (MSSA and MRSA) Historically associated with super absorbent tampons (70’s - 80’s) Can affect men, women (even postmenopausal) and children Risk factors include skin wounds (burns) and surgery  Staph Epidermidis “Gram Positive” Staph Epidermidis “S. epidermidis ” Part of Normal skin flora Immune Compromised patients at higher risk of pathogenic infection Usually, hospital acquired Infects prosthetics devices and indwelling catheters (PICC lines) Bio-films Endocarditis Valves Diagnosis: Blood Culture Positive Signs of infection Treatment: Antibiotics (IV 4-6 weeks) Remove the device  Staphylococcus Saprophyticus “Gram Positive” Staph Saprophyticus “S. saprophyticus” “Urinary tract” Found in the normal flora of the female genital tract and perineum 10–20% of urinary tract infections (UTIs) In females 17–27 years old Second-most common cause of community-acquired UTIs, after Escherichia coli Capacity to selectively adhere to human urothelium Clinical Presentation: Most cases occur within 24 hours of sex – earning this infection, the nickname "honeymoon cystitis“ Burning sensation when passing urine Urge to urinate more often than usual ‘Dripping effect' after urination Razor-like pains during sexual intercourse Treatment: Antibiotics  Review 3 Major Types of Staphylococcus Infections S. Aureus Many types of infections Skin / Soft tissue S. Epidermidis Indwelling prosthetic devices Joints Catheter Heart valves S. Saprophyticus UTI in sexually active women Streptococcal Infection “Gram Positive”  Streptococcal Infection “Gram Positive” Gram Positive bacteria arranged in pairs or chains “can appear bent or twisted” Most streptococci are: Many are facultative anaerobes (Growth both aerobically and anaerobically) Species of Streptococcus are classified based on their hemolytic properties Alpha-hemolytic Oxidization of iron in hemoglobin molecules within red blood cells Greenish color on blood agar Beta-hemolytic Complete rupture of red blood cells Wide clear areas on blood agar Gamma-hemolytic No hemolysis  Streptococcus Pyogenes Disease Pyogenic Pharyngitis Scarlet Fever Sandpaper rash Strawberry tongue Impetigo Cellulitis Toxigenic Toxic Shock-like syndrome Immunogenic Rheumatic fever M protein antibodies Acute Glomerulonephritis  Strep Throat Steptococcal Pharyngitis “S. Pyogenes” “Gram Positive” Group A Beta hemolytic is the MOST COMMON cause of Pharyngitis Group A Strep (GAS) Strawberry tongue Onset: Fever Tender anterior cervical adenopathy Lack of cough Tonsillar exudate Strawberry tongue Scarlatina “Looks like Absence of common cold symptoms (rhinorrhea) sandpaper” Rash-likely scarlatina from erythrogenic toxins (Scarlet fever) The strep bacteria make a toxin that causes a bright red, bumpy rash. The rash spreads over most of the body and is what gives scarlet fever its name  Steptococcal Pharyngitis “Gram Positive” Diagnosis: Increased WBC count with Neutrophils Rapid strep test and culture Transmission: Respiratory droplets from an infected person Directly or by touching something that has droplets on it then touching mouth, nose, or eyes Treatment: Antibiotics PCN/Amoxicillin/Augmentin COMPLICATIONS 1. Otitis media 2. Sinusitis 3. Abscess 4. Glomerulonephritis 5. Rheumatic Heart Disease Molecular mimicry  Strep Skin Infection “S. Pyogenes” “Gram Positive” Strep is NOT normal skin flora Infections are secondary to colonization Strep SPREADS through tissues Staph is LOCALIZED Diagnosis and Treatment: Cultures: Wound and Blood cultures are positive for Group A strep Antibiotics: PCN Keflex (1st generation cephalosporin) Clindamycin (lincosamides)  Pneumococcal Pneumonia (Streptococcus Pneumoniae) S. pneumoniae “lancet-shaped diplococci” Gram-positive Facultative anaerobe IgA protease Destroys IgA Alpha-hemolytic Under aerobic conditions  Pneumococcal Pneumonia (Streptococcus Pneumoniae) Pathogenesis: Spreads by direct person-to-person contact via respiratory droplets Clinical Presentation: Most common type of community-acquired pneumonia Bacterial pneumonia found in adults Key Features of the Capsule 1.Composition: The capsule is made up of polysaccharides and varies among different Meningitis strains 2.Virulence: The capsule helps resist Neonatal infections phagocytosis by immune cells, allowing the Presentation & Diseases: bacteria to survive and multiply within the Otitis Media Sepsis in patients with host Splenectomy 3.Clinical Implications: The presence of the Sinusitis Rusty sputum capsule is a key factor in the pathogenesis of diseases caused by S. pneumoniae, such as pneumonia, meningitis, and otitis media. MOPS Meningitis 4.Vaccination: Pneumococcal vaccines, such Otitis Media as the polysaccharide and conjugate Pneumonia vaccines, target the capsule to provide immunity against the most common  Pneumococcal Pneumonia (Streptococcus Pneumoniae) Signs and Symptoms Productive cough Fever Pleuritic Pain Sputum – red or rusty Diagnosis CXR- Lobular infiltrate or consolidation Sputum and blood culture - 80-95%  Pneumococcal Pneumonia (Streptococcus Pneumoniae) Treatment: Penicillin Cephalosporin (2nd or 3rd generation) Macrolide - Clarithromycin “Biaxin” Fluoroquinolones - Levaquin Prevention: Vaccinate, Vaccinate, Vaccinate!!!!! Two kinds of pneumococcal vaccines are used in the United States help protect against pneumococcal disease: Pneumococcal conjugate vaccines (PCV13, PCV15, or PCV20) Pneumococcal polysaccharide vaccine (PPSV23) In the polysaccharide vaccine, only the sugar part of the bacteria, the capsule, is included as the antigen to stimulate the immune response. In the conjugate vaccine, it's actually the sugar joined to the carrier protein. Conjugate has greater immunogenicity but narrower spectrum of pneumococcal serotypes  Pneumococcal Meningitis “Bacterial Meningitis” Etiology: CSF leak Pneumonia Sinusitis Head trauma Signs and symptoms: Fever Headache Meningismus (neck rigidity) Mental status changes No rash!!!  Pneumococcal Meningitis “Bacterial Meningitis” Lumbar Puncture (LP) for diagnosis Bacterial Clear, cloudy or purulent fluid Opening pressure ELEVATED Decreased GLUCOSE Increased PROTEIN >100 WBC - > 90% neutrophils Viral (Aseptic) ✓ Clear fluid ✓ Opening pressure normal or elevated ✓ Increased GLUCOSE ✓ Increased PROTEIN ✓ 10-1000 WBC - Low neutrophils  Clostridium Species Rod-shaped Gram-positive bacteria Obligate Anaerobes Don’t do well with oxygen Grows in the absence of oxygen Produces Endospores Enable bacteria to lie dormant for extended periods Alpha Toxin Lecithinase Phospholipase…destroys cell membranes RBC, WBC, muscles Inhabit soils and Intestinal tract  Clostridium Species Clostridium causes several significant human pathogens including: Clostridium Perfringes Food poisoning Clostridium septicum Gas Gangrene Clostridium tetani Tetanus Vaccine Clostridium botulinum Botulinum toxin in foods Botox Clostridium difficile Antibiotic associated diarrhea When normal flora is destroyed by Antibiotics  Clostridium Perfringes Present in: Soil Raw Meat and Poultry Most common cause of food poisoning Stews, casseroles, and gravy Food whose temperature is poorly controlled Signs and Symptoms: Abdominal Pain Diarrhea Starts within 6-24 hours (Usually lasts less than 24 hours) Fever & Vomiting NOT normally symptoms Treatment: Rest Fluids Education Food Safety (maintain a temperature of 140)  Clostridium Difficile Causes life-threatening diarrhea Usually, a side-effect of taking antibiotics!! These infections mostly occur in:  People 65 and older who take antibiotics and receive medical care  People staying in hospitals and nursing homes for a long period of time  People with weakened immune systems or previous infection with C. diff Symptoms might start within a few days or several weeks after you begin taking antibiotics Diarrhea: loose, watery stools (poop) for several days Fever Stomach tenderness Loss of appetite Nausea C. diff can easily spread from person to person C. diff is a major health threat. In 2017, there were an estimated 223,900 cases in hospitalized patients and 12,800 deaths in the United States [ Source: 2019 AR Threats Report].  Clostridium Difficile Alcohol-based hand sanitizers are highly effective against non–spore-forming organisms, but they DO NOT kill C. difficile spores or remove C. difficile from hands  Clostridium Tetani (Lock Jaw) Found in soil Gain entry through wound Nail puncture Toxin interferes with neurotransmitter at spinal synapses Renshaw cells “Inhibitory interneurons found in the gray matter of the spinal cord” Incubation 5 days to 15 weeks ~ 8-12 days Diagnosis: Violent muscle spasms Trismus “lockjaw” Increased reflexes Respiratory failure  Clostridium Tetani (Lock Jaw) Treatment: Human Tetanus Immunoglobulin (TIG) PCN to eradicate any bacteria Benzodiazepines to treat muscle spasms Prevention:  VACCINATE  VACCINATE  VACCINATE  Clostridium Botulism Spores in soil Contaminate vegetables and meats No honey in infants Canned or vacuumed spores survive Germinate in anaerobic environment Resistant to degradation by enzymes found in the gastrointestinal tract Allows ingested toxin to be absorbed from the intestines into the bloodstream Released neurotoxin Inhibits acetylcholine release Parasympathetic Ganglia Neuromuscular junction Symmetric paralysis within 12-72 hours after exposure Most potent toxin known to humankind Has been used now as Botox………  Clostridium Botulism Clinical Presentation:  Descending flaccid paralysis  Diplopia  Ptosis  Floppy baby  Constipation cdc.gov  Clostridium Botulism Clinical Presentation:  Descending flaccid paralysis  Diplopia  Ptosis  Floppy baby  Constipation Signs and Symptoms: 5 D’s 1. Diplopia (double vision) 2. Dysphonia (inability to produce voice sounds) 3. Dysarthria (difficult to pronounce words) 4. Dysphagia (difficulty swallowing) 5. Descending paralysis of facial muscles Treatment: A trivalent (types A,B,C) equine serum toxin Supportive care with mechanical ventilation Debridement of wound Clostridium Botulism  Botulinum: Anti-spasticity effects for therapy Injected into selected muscle(s) Relaxation/paralysis occurs within 3 to 7 days: lasts 2 to 3 months It doesn’t ware off……. The nerve will re-sprout and crate a new presynaptic terminal Muscle will respond to the new Ach Reduces spastic dominance…….may allow: Increased residual function Improved ADL, Bracing AFO, etc…  Bacillus anthracis Anthrax Gram positive Rod Aerobic Spore forming Spores are in soil on animal product hides, bristle and wool of infected animals 3 types Cutaneous anthrax Occurs 2 weeks after exposure to spores Large, Painless ulcer with black eschar and surrounding edema Inhalation anthrax Lung infection Resulting sepsis Gastrointestinal anthrax Exposure to meat products with spores Nausea, vomiting, diarrhea and fever  bacterium Corynebacterium diphtheriae “Diphtheria" Gram positive Club shaped rod Humans only natural host Aerobic Transmission: Via inhalation Open skin  bacterium Corynebacterium diphtheriae “Diphtheria" Clinical Presentation: Upper Respiratory Infection “URI" Sore throat Nasal discharge Malaise Hallmark Sign: Sheet of thick, gray material covering the back of your throat Which can block your airway Causing you to struggle for breath Complications: Myocarditis Laryngeal palsy “dysphagia"  bacterium Corynebacterium diphtheriae “Diphtheria" Diagnosis made clinically and confirmed by culture Prevention Vaccinate Childhood immunization with booster Treatment Antitoxin (from horses) Penicillin or macrolide  Listeria monocytogenes “Listeriosis" Gram positive Rod Grows intracellular in host Facultative anaerobic Does NOT produce endospores Listeriosis can cause serious illness Pregnant women Newborns Immunocompromised Elderly May cause gastroenteritis in others who have been severely infected Transmission via contact with: Animal Feces Unpasteurized Dairy Contaminated Vegetables  Listeria monocytogenes “Listeriosis" Healthy people rarely become ill from listeria infection People with weakened immune systems are at higher risk of life- threatening complications Listeria bacteria can survive refrigeration and even freezing DANGER Pregnancy-toxic to the fetus Most at risk unborn babies and newborns (fatal) Immunocompromised patients (transplants) Watch out for soft cheeses or dairy that has not been pasteurized Treatment: Antibiotics Gram Positive Bacteria “Review” Gram NEGATIVE Bacteria  Escherichia coli Gram-negative Rod-shaped bacterium Facultative aerobic Found in the lower intestine Benefit hosts by producing vitamin K2 Most strains are harmless but some strains cause: Food poisoning Pneumonia Urinary tract infections 75% to 95% of UTIs are caused by E. coli  Escherichia coli Some strains of E. coli makes you sick by making a toxin called Shiga Toxin damages the lining of your intestine Under cooked meat Unpasteurized milk Petting Zoo’s (Fairs) Improper Fecal Oral Hygiene Escherichia coli O157:H7 strain “Typically foodborne illness” Transmission is via the fecal–oral route Shiga toxin–producing types abdominal cramps, vomiting, and bloody diarrhea Leading cause of acute kidney failure in children HUS: This serious condition is characterized by the triad: 1. Hemolytic anemia 2. Acute kidney injury 3. Thrombocytopenia (low platelet count)  Pasteurella multocida Gram-negative Coccobacillus Non-motile Cause a zoonotic infection in humans Result of bites / scratches or licks from domestic pets Many mammals (domestic cats, dogs & birds) harbor it as normal mouth & respiratory microbiota Most prevalent bacteria present in domestic and wild animals worldwide Aggressive Skin manifestations typically appear ~ 24 hrs following bite Fairly sensitive organisms Treated with a penicillin-based regimen (Augmentin)  Eikenella corrodens “Fight Bite” Gram Negative Appears coccobacillary Anaerobic bacillus Eikenella corrodens is a commensal of the human mouth & upper respiratory tract Infection does NOT become clinically evident until a week or more after the injury Needle-licker's osteomyelitis HACEK Organisms Group of gram-negative bacteria that cause culture-negative endocarditis Haemophilus Aggregatibacter (previously Actinobacillus) Cardiobacterium Eikenella Kingella Treatment:  Bordetella Pertussis “Whooping Cough" Small gram negative Coccobacilius Aerobic NOT motile Transmission: Airborne droplets Direct contact with infectious discharge Incubation 7-17 days Most common in children less then 2 years old  Bordetella Pertussis “Whooping Cough" Diagnosis: Nasal culture Takes 7-10 days to grow PREVENTION: VACCINATE All infants and mothers, caretakers Treatment: Antibiotics (macrolide)  Neisseria Meningitidis “Meningococcal Meningitis" Gram negative Diplococci Often referred to as meningococcus Cause Meningitis and other forms of meningococcal disease Meningococcemia “Life-threatening sepsis” Main cause of bacterial meningitis in children and young adults Developmental impairment Death in ~ 10% of cases N. meningitidis spread through saliva and respiratory secretions: Coughing Sneezing Kissing Chewing on toys Sharing a source of fresh water  Neisseria Meningitidis “Meningococcal Meningitis" Pathogenesis: Infects host cells by sticking to them with Long thin extensions called pili Who is at Risk? Children under 5 Young adult (think college age) Immune deficiency Signs and Symptoms High fever Headache Purpuric Rash Confusion  Neisseria Meningitidis “Meningococcal Meningitis" Diagnosis: Lumbar puncture  Shows Low glucose and High protein  Gram stain of LP fluid shows (Gram Negative staining)  Culture Chocolate agar plates Treatment: Antibiotics PREVENTION ….Better than treatment VACCINATE Breast Feeding for 6 months  Haemophilus Influenzae “H. flu” Gram-negative Capsule Coccobacillary Facultative anaerobe Bacterium was mistakenly considered to be the cause of influenza until 1933 Still colloquially known as bacterial influenza Presence of the capsule in encapsulated type b (Hib) known to be a major factor in virulence Allows resistance to phagocytosis and complement-mediated lysis Entry through upper respiratory tract Causes: Sinusitis Epiglottitis Otitis media Pneumonia Meningitis  Haemophilus Influenzae “Epiglottitis” Epiglottitis: Abrupt onset of fever Inability to control oral secretions AIRWAY OBSTRUCTION MEDICAL EMERGENCY Diagnosis: Direct Laryngoscopy X-ray (thumb print sign) Treatment: Antibiotics Supportive care Intubation-especially children  Meningitis “H. Flu" Upper Respiratory infection Stiff neck Treatment: Antibiotics  Legionella pneumophila "Legionnaire’s Disease" Gram negative (faint staining) Thin Rod Aerobic Flagellated Legionella acquired its name after an outbreak of an unknown "mystery disease" sickened 221 persons, causing 34 deaths Outbreak was first noticed among people attending a convention of the American Legion(association of U.S. military veterans) Associated with Environmental Water sources  Legionella pneumophila "Legionnaire’s Disease" Signs and Symptoms: Nonproductive cough Confusion Diarrhea Nausea and vomiting Fever Lab diagnosis: CXR: Focal patchy infiltrates Culture: Chocolate Agar-> Legionella Antigen TREATMENT: Antibiotics  Salmonella "Salmonellosis” Gram Negative Rod Nonspore-forming Motile Peritrichous flagella “All around the cell body” Facultative aerobes Two species of Salmonella: 1.Salmonella bongori Cold-blooded animals “reptiles” 2.Salmonella enterica “Several subspecies” Warm-blooded animals Environment  Salmonella "Salmonellosis” Salmonellosis - Symptomatic infection caused by bacteria of the Salmonella type Salmonellosis is one of the most common causes of diarrhea globally Typically occurs between 12 - 36 hours after exposure Symptoms lasting from two to seven days Spread by eating contaminated meat, eggs, or milk Most common symptoms: Diarrhea Fever Abdominal cramps Vomiting Dehydration  Salmonella "Salmonellosis” Disease caused by Salmonella serotype Typhi bacteria 1. Enteric fever or Typhoid fever: - Transmitted through contaminated food or drink (dairy or poultry) - Infects intestines-> lymphatics->rest of organs - Incubation 5-14 days Signs and Symptoms: - Malaise - Sore throat - Low grade fever - Diarrhea (pea soup) Culture?- Early stages Treatment: Quinolone (Cipro)  Shigella Gram negative “Shigellosis" Rod Facultative aerobe Shigella causes disease only in primates Transmitted by fingers, flies, food and feces Fecal-oral Incubation 1-4 days Signs/Symptoms: Bloody, mucoid diarrhea High fever Abdominal cramps Diagnosis: Stool Culture Treatment: Mild cases Supportive (rehydration, rest) Severe cases Antibiotics Quinolone (Cipro)  Vibrio Cholera Gram negative (Curved Rod “Looks like a Comma“) Facultative anaerobe Flagellum Bacterium's natural habitat is brackish or saltwater V. cholerae cause the disease cholera Incubation 11-72 hours Human only affected Transmission via food and water Areas of poor sanitation-Central America, Africa Signs and Symptoms: Profuse "rice-water" diarrhea Severe dehydration Diagnosis: Culture: Stool Treatment: Supportive care (rehydration) Antibiotics  Francisella tularensis “Tularemia / “Rabbit fever” Gram-negative Rod-shaped Coccobacillus Aerobic Causative agent of tularemia “Typically spread by ticks, deer flies, or contact with infected animals” Reservoir: Rabbits, Beavers, Hamsters Signs/Symptoms: Ulcer or papule at site of penetration High fever (104) Nausea, malaise, headache, pneumonia Diagnosis: Blood cultures Serum antibodies rise in 2nd week Treatment: Antibiotics  Yersinia pestis Gram-negative Plague Rod-shaped "Ring around the Rosie" Nonmotile Coccobacillus Facultative anaerobe  Causes the Plague Three main forms: 1. Pneumonic - Pulmonary 2. Septicemic - Blood 3. Bubonic plagues - Lymph nodes  Yersinia pestis Plague Transmission: Rodents…..flea bites (1-7 days) Infected human….. Airborne droplets (2-4 days) Signs/Symptoms: Fever, malaise, sore throat, myalgias Lymphadenopathy inguinal area Bubonic lesion at site of entry Diagnosis: Blood cultures Treatment: Antibiotics Prevention: VACCINATE!!! Traveling or military  Neisseria gonorrhoeae “Gonococcal Infections" Gram negative Diplococci Gonorrhea Transmission: Sexually transmitted disease (STDs) and Perinatal Men: Dysuria and milky discharge Women: Dysuria and milky discharge - can by ASYMPTOMATIC When it goes untreated: BAD!...can become disseminated Purulent arthritis o Triad 1. Rash 2. Synovitis 3. Arthralgias Conjunctivitis: Babies through the birth canal  Neisseria gonorrhoeae “Gonococcal Infections" Symptoms: Urethritis, Pharyngitis, Conjunctivitis Males: Epididymitis, prostatitis Female: Cervicitis, PID Diagnosis: Cultures: Men: Urine Women Cervical (can do urine) Treatment: we treat for both gonorrhea and chlamydia Antibiotics Prevention: 1. Condoms 2. Abstinence 3. Know your partner! 4. Frequent testing  Chlamydia Trachomatis “Chlamydia” Gram negative Ovoid shape Nonmotile Transmission: Sexually transmitted disease (STDs) and Perinatal Lesions on genitalia (Cervicitis or Urethritis) Lymph Nodes 1-4 wks Diagnosis: Cultures: Men: Urine Women Cervical (can do urine) Treatment: we treat for both gonorrhea and chlamydia Antibiotics Chlamydia Trachomatis “Chlamydia” Chlamydia Trachomatis “Chlamydia” Men Women Up to date (2016)  Chlamydia Trachomatis “Chlamydia” DNA Testing: Nucleic acid amplification testing (NAAT) is the recommended method for initial screening or testing for Chlamydia trachomatis (CT) and Neisseria gonorrhoeae (NG) infections. Swab Urine Prevention: 1. Condoms 2. Abstinence 3. Know your partner! 4. Frequent testing  Infective Endocarditis Invasion of the heart valve or endocardium Leading to colonization and eventual destruction of the cardiac tissue Risk factors: IV drug use (staph aureus) Structural heart abnormalities (prosthetic heart valve) Signs/Symptoms: Low grade temperature (most common 90%) Malaise Physical Exam: New cardiac murmur Heart failure EKG changes with conduction abnormalities Splinter hemorrhages Osler nodes “Ouch” Janeway lesions Roth spots “hemorrhage from retinal blood vessel)  Infective Endocarditis Diagnostic Tests Modified Duke Criteria- MAJOR 1. Blood culture 2. Echocardiogram 3. Murmur 1) Two separate positive blood cultures with microorganisms typical for infective endocarditis Streptococci Viridans Streptococci Bovis Staph aureus Community Acquired Enterococci HACEK: Haemophilus, Actinobacillus, Cardiobacterium hominis, Eikenella corrodens, Kingella 2) Echocardiographic evidence of endocardial involvement (TEE) Vegetation Abscess New partial dehiscence of a prosthetic valve (Within 2 months) 3) New valvular regurgitation Increase/change in pre-existing murmur not sufficient  Infective Endocarditis Diagnostic Tests Modified Duke Criteria- Minor Predisposition: Predisposing heart condition Current prosthetic heart valve or a valve lesion IV drug use Fever Temperature greater then 38 C (100.4 F) Immunological phenomena: Glomerulonephritis, Osler nodes, Roth spots, Rheumatoid factor Microbiological evidence: + blood culture BUT NOT meeting major criteria Serologic evidence of active infection with an organism consistent with infective endocarditis Vascular phenomena: Major arterial emboli Septic pulmonary infarcts Infective Endocarditis  TTE vs. TEE TTE (transthoracic echocardiogram) First diagnostic test for patients with suspected IE Sensitivity is modest (up to 75 percent) Specificity approaches 100 percent TEE (transesophageal echocardiography) Sensitivity of >90 percent for detection of valvular vegetation Superior to TTE for detection of cardiac complications such as: - Abscess - Leaflet perforation - Pseudoaneurysm Gram NEGATIVE Bacteria “Review”  Mycobacterium Tuberculosis “Tuberculosis” Coating makes the cells impervious to Gram staining For identification use Acid-fast stains such as Ziehl-Neelsen Fluorescent stains such as auramine Primarily attacks the lungs but can attack kidney, brain and spine Transmission: Humans-> via air (coughing, sneezing, singing, speaking) Not by hand shaking Signs/Symptoms: Prolonged cough for 3 weeks, chest pain, bloody sputum Weakness, chills, weight loss, fever Define/classify: Location: Pulmonary Extrapulmonary Activity: Active Latent  Mycobacterium Tuberculosis “Tuberculosis” Pulmonary Tuberculosis: Tuberculosis (TB), formerly known as Consumption Infectious, inflammatory systemic disease affecting the lungs: May disseminate to involve lymph nodes and other organs Characterized by: Granulomas- (an organized collection of macrophages) Caseous {kā-sē-əs} (resembling cheese) necrosis Combination of coagulative and liquefactive necrosis Subsequent cavity formation  Mycobacterium Tuberculosis “Tuberculosis” Pulmonary Tuberculosis: First or primary infection with the tubercle bacillus is usually asymptomatic Secondary TB, most common form of clinical TB, Result of either endogenous or exogenous reinfection Reactivated TB usually causes abnormalities in upper lobes of lungs Can also move to joints……. Why the Apex???? More oxygen…..less profusion  Mycobacterium Tuberculosis “Tuberculosis” Pulmonary Tuberculosis: TB remains a global health problem with the highest rates in Southeast Asia, sub-Saharan Africa, and eastern Europe New cases 200 to 400 per 100,000 Multidrug-resistant TB has emerged as a major infectious disease problem Although TB can affect anyone, certain populations at higher risks:  HIV infection  People age 65 years and older  Economically disadvantaged or homeless  People living in overcrowded conditions  Hispanics, Native Americans, and Asian/Pacific Islanders  Clients dependent on injection drugs, alcohol  Infants and children under the age of 5 years  People with diabetes mellitus  Mycobacterium Tuberculosis “Tuberculosis” Pulmonary Tuberculosis: Causative agent: is tubercle bacillus Commonly transmitted in the United States by: Inhalation of infected airborne particles, known as droplet nuclei Produced when the infected persons sneeze, laugh, speak, sing, or cough Casual contact or brief exposure to a few bacilli will not result in infection Tubercle bacillus is capable of surviving for months in sputum Within the body it becomes encapsulated and can lie dormant for decades Become reactivated years after an initial infection Once a susceptible person inhales droplet nuclei containing M. tuberculosis and bacilli become established in the alveoli of the lungs, a proliferation of epithelial cells surrounds and encapsulates the multiplying bacilli in an attempt to wall off the invading organisms, thus forming a typical tubercle  Mycobacterium Tuberculosis “Tuberculosis” Pulmonary Tuberculosis: Often symptoms are delayed until 1 year or more after initial exposure Symptoms include productive cough of more than 3 weeks’ duration, especially when accompanied by other symptoms such as weight loss, fever, night sweats, fatigue, malaise, and anorexia Medical management: Preventing the transmission is essential and can be done by: Covering the mouth and nose with a tissue when coughing and sneezing Diagnostic measures currently include: History Physical examination Tuberculin skin test Chest radiograph Microscopic examination Culture of sputum  Mycobacterium Tuberculosis “Tuberculosis” Pulmonary Tuberculosis: Medical management: Tuberculin skin test Most common method currently used that demonstrates infection with M. tuberculosis in the absence of active TB Pharmacologic treatment through medication is the primary treatment of choice Renders the infection noncontagious and nonsymptomatic Tuberculin Skin Test Mycobacterium Tuberculosis “Tuberculosis”  Drug Therapy for Initial Phase of TB RIPE 1. Rifampin 2. Isoniazid 3. Pyrazinamide 4. Ethambutol  Mycobacteria (Nontuberculous) Mycobacterium Marinum: Free-living bacterium Causes opportunistic infections in humans Disease known as aquarium granuloma which typically affects individuals who work with fish or keep home aquariums Salt water and fresh water Swimming pool exposure to non chlorinated water Nodular skin lesions Treatment: Antibiotics Mycobacterium avium complex (MAC) Most common bacterial infection in HIV/AIDs Found in water and soil X-ray-> indistinguishable from TB Treatment: Antibiotics  Spirochetes General Characteristics: Group of bacteria characterized by their unique spiral shape Flexible spirally twisted bacterium Spirochetes are the cause of syphilis and Lyme disease Generally regarded as Gram negative bacteria, because they have a thin peptidoglycan layer Gram staining is NOT commonly used to stain them as they do not take up the stain well Silver stains are typically used to identify spirochetes  Syphilis Treponema pallidum is a spirochete that can affect almost any organ or tissue Transmission occurs most frequently during sexual contact There has been a rising incidence of the disease in urban areas Adolescents and young adults Injection drug users Syphilis can have 3 stages to the infection Primary Presents with a painless single chancre Secondary Presents with multiple cutaneous lesions “rash” Tertiary Presents with systemic involvement and neuro symptoms Early infectious (primary and secondary) and late (tertiary) syphilis are separated by a symptom-free latent phase, during which the infectious stage may recur  Primary Syphilis  Caused by the spirochete Treponema pallidum Transmission: Direct contact / sexual activity Presentation: Painless genital lesion “punchout appearance” 3 week to 3-month incubation phase Chancre (which will heal on its own) Heals within 3-6 weeks Diagnostic Studies: Darkfield microscopy (technique is difficult) Demonstrate T. pallidum in material from suspected lesions Revealing outlines, edges, boundaries, of organisms  Primary Syphilis  Caused by the spirochete Treponema pallidum Management: Antibiotics Single IM injection of Benzathine Penicillin G Even in Penicillin-allergic patients (you can adjust administration) Special Notes: Syphilis has the painless ulcer (chancer) Painless ulcer with a clean base and firm, indurated margins. Develops at the site of inoculation, most commonly the genital area Regional lymphadenopathy (rubbery, discrete, nontender) Chancre on the underside of the penis  Secondary Syphilis  Caused by the spirochete Treponema pallidum Transmission: Direct contact / sexual activity Presentation: Rash on pals and soles Sexually active with a history of Painless genital lesion 5-8 weeks ago Diagnostic Studies: VDRL and RPR They detect nonspecific antibodies that may indicate syphilis Tests are divided into:  Non-treponemal tests (RPR or VDRL) Typical presentation of secondary syphilis with a rash on the palms of Reddish papules and nodules over  Treponemal-tests (FT-ABS, TPPA, MHA-TP) the hands much of the body due to Testing for syphilis can begin with a non-treponemal test secondary syphilis If these tests are negative, syphilis may be ruled out Because of the possibility of false positives with non-treponemal tests, if the initial test is positive, confirmation is required with a treponemal test. If that test is positive as well, then the diagnosis of syphilis is confirmed.  Secondary Syphilis  Caused by the spirochete Treponema pallidum Management: Antibiotics Single IM injection of Benzathine Penicillin G Even in Penicillin-allergic patients (you can adjust administration) Special Notes: Rash may start on trunk and spread outwards Jarisch-Herxheimer reaction Acute febrile reactions accompanied by headache and myalgias within 24 hr after treatment Release of endotoxin-like substances when large numbers of Treponema pallidum are killed by antibiotics Cytokine storm  Tertiary Syphilis Late (tertiary) syphilis includes gummatous (soft, non-cancerous) lesions involving: Skin Bones Viscera cardiovascular disease Nervous system and ophthalmic lesions Tabes dorsalis Is a late manifestation of untreated syphilis Primarily affects the dorsal columns of the spinal cord and the nerve roots  Sensory Ataxia  Pain Patient with tertiary  Loss of DTR (gummatous) syphilis. Bust in  Argyll Robertson pupil (they accommodate, but do not constrict to light) Musée de l'Homme, Paris. All cases of syphilis must be reported to the appropriate public health agency for contact tracing Careful follow-up is essential to monitor the effectiveness of treatment and to identify treatment failures HIV testing and screening as well as treatment of concurrent sexually transmitted diseases should be done  Reportable 1. Sexually Transmitted Infections (STIs): 4. Gastrointestinal Syphilis Infections: Gonorrhea Salmonellosis Chlamydia Shigellosis HIV/AIDS Campylobacter infection 2. Vaccine-Preventable Diseases: 5. Vector-Borne Diseases: Measles Lyme disease Mumps West Nile virus Rubella Zika virus Hepatitis A and B 6. Others: 3. Respiratory Infections: Legionnaires' disease Tuberculosis (TB) Candidiasis (certain types) Influenza-associated hospitalizations Rheumatic fever COVID-19 (in many areas) Each state or country may have its own specific list, so it's essential to consult local public health guidelines for the exact requirements. Reporting helps track outbreaks and informs public health responses.  References Text: Current Medical Diagnosis & Treatment Text: Cecil’s Essentials Rosh Review Rapid review pulmonology Wolf, Oslie, Rosh 2019