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Micro ID #2: Bacterial Diseases and Vaccination

Micro Id #2: Bacterial Diseases And Vaccination

by ibp2102, Apr. 2012

Subjects: micro

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	What do "sequestrum" and "involucrum" mean in the context of bone infections (osteomyelitis)?	Sequestrum = necrotic bone (from compression/ischemia of blood vessels by purulence and inflammation) Involucrum = bone deposition, new bone that's formed under periosteum
	Clinically and Histologically, how can we distinguish between Acute and Chronic osteomyelitis?	Clinically- Acute: first clinical episode Chronic: recurrent episode HistoPath- Acute: acute inflammation of bone Chronic: necrotic bone
	What is the most common form of osteomyelitis in children?	Hematogenous (spread from blood) In general ~20% of cases
	What is the most frequent site of hematogenous osteomyelitis in: Kids Adults	Kids- long bones (ex: femur, tibia, humerus) Adults- spine (vertebral body and disk space, Lumbar and Thoracic)
	What are the three classifications of osteomyelitis?	- Hematogenous - Secondary to contiguous focus OR direct inoculation - Associated with vascular insufficiency
	At what age does the epiphyseal plate close? Till what age should parents be concerned about impaired growth for their child with osteomyelitis?	Epiphyseal plate closes at 1 years and will prevent spread of infection, not affecting growth. Earlier than 1- can affect growth.
	Describe the steps leading up to involucrum in long-bone pediatric osteomyelitis.	-Infection starts at metaphysis (most vasculature) -It spreads laterally - Perforates cortex and lifts periosteum - New bone is deposited (involucrum)
	How do gram- bacteria from the urinary tract cause osteomyelitis in older men?	They can come through the Batson's venous plexus (aka prostatic venous plexus) and reach the spine.
	What is the most common bacterial culprit causing hematogenous osteomyelitis?	Staph aureus (60-90%) Neonates- group B strep Children- group A strep Adults- S. aureus IV drug users- Pseudomonas, Serratia
	What are some signs that a person has osteomyelitis? Will neurological findings be frequently present	Localized pain, decreased RANGE OF MOTION Fever, chills erythema NOT common to see neurologic findings. Only if possibly epidural abscess pushes into spinal chord/peripheral nn.
	In what age population does osteomyelitis secondary to a contiguous focus most frequently occur? What specific bones does it target if any?	Most frequently in adults. May involve any bone
	A person is bitten by their cat and develops terrible pain and swelling in their finger joint where the cat bit them. There is visible redness and examination reveals osteomyelitis. What pathogen would you expect if the wound site was cultures?	Pasteurella multocida (from Cat bite)
	What patient's are at greatest risk for osteomyelitis associated with vascular insufficiency?	Diabetes They can get neuropathies and increased infection of soft tissue of foot that can spread.
	What is the most likely organisms causing early stages of diabetic osteomyelitis? What are he most likely organisms causing vascular insufficiency osteomyelitis?	Early- Staph/ Strep Middle: staph/strep and gram - Poor diabetic control- staph/strep gram - and anaerobes
	T of F A simple blood culture from the site of bone infection is enough to diagnose a patient alone.	False! No one test can confirm or exclude a diagnosis Blood tests (nonspecific inflammation) X-rays (take 10 days to return!) CT/MRI Culture Histology/ Pathology
	How do you treat osteomyelitis after cultures are taken?	Antibiotics- HIGH dose, looooooooong 4 weeks or more, bacteriCIDAL Surgery- for debridement and possible amputation Surgery
	Can cartilage be replaced? In what time frame did this BEGIN to happen?	Yes! Destruction of articular cartilage begins within 48 hrs (2 days)
	What is the most common pathogen causing joint infection in Adults? What is the most common........Adults?	<40 = Neisseria gonorrhoeae >40 Staphylococcus aureus
	If you could use only one test for diagnosing blood cultures of someone with suspected joint infections, what would it be?	Joint fluid- gram stain and culture!
	What is the appropriate treatment for Joint infection?	DRAINAGE (and also IV antibiotics help)
	What is infective endocarditis?	infection of endocardial surface of heart and heart valves. (can sometimes include large blood vessels and affect previously formed holes in heart)
	What is the difference between acute and subacute endocarditis?	Acute: rapid, fulminating, fatal within several weeks. Affects NORMAL valves Subacute: affects PREVIOUSLY DAMAGED valves (can cause sxs for months)
	What age group is mostly affected by infective endocarditis (IE)?	People over age 50
	What types of conditions put a person at risk for IE?	- Prosthetic heart valve - IV drug use - Degenerative conditions involving heart valves: ex - hypertrophic cardiomyopathy - Prior hx of IE - mitral valve prolapse
	Describe the pathogenesis of IE	1. Damage to endothelium (turbulence, trauma, etc.) leads to platelet aggregation and thrombus formation 2. Transient bacteria colonize the thrombus- form vegetation 3. vegetation enlarges and organisms continue to grow
	What is a vegetation?	It is a collection of bacteria or other organisms growing within a thrombus.
	Which side of the heart is most affected by IE? Accordingly, which valves do you expect get the most vegetation?	L side (because it pushed larger volume of blood out, it gets most pressure and turbulence) Mitral valve 85% and aorta 55% tricuspid 0-6% (more seen in IV drug use)
	What systemic manifestations of IE would you expect?	- splenic infarct (heart immediately sends blood to spleen) - MCA emboli --> cerebral infarct - glomerulonephritis (immune complex deposition) -mycotic aneurysm
	What organisms are responsible for the majority of IE cases?	- streptococci and enterococci 40-50% - staphylococci 40-5-% - gram neg. bacilli 2-10% - gram pos., Fastidious gram - (HACEK) uncommon
	What are the clinical manifestations that suggest IE?	FAME= Fever (majority, 80%) Anemia Murmur (85-95% of cases) Emboli Also can present with Arthralgias, myalgias. RUQ pain (suggesting splenic involvement). Skin findings: splinter hemorrhage, petechiae, etc.
	What are some embolic phenomena that might be visible in a patient with IE?	Splinter hemorrhages (linear nail-bed lesions) Petichiae (uncommon) Osler's nodes (finger pads) Janeway's lesions (palms and soles) Roth Spot (retina, red hemorrhagic lesion with white central spot) Cerebral emboli
	Which organisms cause IE in intravenous drug abusers? What valve is most affected in IV drug users?	S. aureus (think of open, lacerated skin being colonized) Pseudomonas Candida and Aspergillus Tricuspid valve (IV drug users tend to shoot up right arm of body)
	T or F Endocarditis in IV drug users can cause pulmonary emboli and pleuritic pain.	True IV drug users tend to have right sided endocarditis which is characterized by multiple pulmonary emboli.
	What laboratory findings would you expect to see in a patient with IE?	1. Erythrocyte sed rate (ESR)- marker of inflammation, elevated 2. Anemia (present in 70-90% of cases) 3. Microscopic hematuria 4. Rhematoid factor Abs seen in pts with subacute endocarditis 5. Not always, but sometimes, elevated WBC
	What is the single most important diagnostic test for diagnosing infective endocarditis?	Blood cultures (awesome if it can be done before starting empiric antibiotics)
	How many sets of blood cultures should be drawn in patients in whom you suspect IE?	Generally at least 3 sets spaced in time Pts. not on antibiotics who get at least 2 blood cultures can have >90% chance of yielding organism
	Besides blood cultures, what other diagnostic tools are used in the treatment of IE?	ECHO (check out blood flow, vegetation) Transesophageal (TEE) is more sensitive and specific BUT more invasive. Transthoracic (TTE) is EASIER but less specificity.
	T or F In a patient who is suspicious for IE, if blood cultures come back negative, it is useful to do an ECHO.	False ECHO is seldom useful if blood cultures come back negative (unless there's super strong evidence to support the diagnosis)
	What type of therapy do patients get put on for IE?	-Long-term IV antibiotics - Surgery (especially if pt has refractory heart failure, abscess, fungal endocarditis, serious emboli, etc)
	Why is a person being treated for IE on antibiotics for 4-6 weeks (long regimen)?	Vegitation is avascular (lack of blood flow means it will be difficult to deliver antibiotics). Short therapy courses are likely to relapse.
	T or F Typically, the antibiotics that treat IE are bacteriostatic drugs?	False They are typically bacteriocidal because bacteria is surrounded by fibrin and phagocytes might not have access to them or might be too plentiful for bacteriocidal drugs to be effective.
	What antibiotic treatment would you use to treat Staph Aureus?	- Nafcillin - if MRSA, use Vancomycin
	Vaccination and Immunization are often used interchangeably. What is the difference between the two?	Vaccination= administrating a vaccine (doesn't guarantee immunization) Immunization = providing immunity against an organism (active or passive, and may not involve vaccine)
	T or F Vaccination is the single most cost effective means of controlling the spread of infectious disease.	True! It is very good for the economy and considered the leading public health achievement of the 20th century.
	What is meant by community or herd immunity?	Removing a disease from individuals in a community helps prevent it's spread to others in a group.
	Which of the vaccine preventable diseases have the most significant worldwide campaign efforts today? What is the leading cause of death among young children of vaccine preventable diseases?	Polio and Measles Measles (vaccine is harder to transport because needs to be cold)
	What is the difference between Active and Passive Immunization? Which is the generally preferred method?	Active= trigger body to produce Abs and other immune mxns. to prevent disease Passive= administer exogenous antibodies to provide temporary treatment/prevention of disease Active is preferred provides prolonged immunity
	T or F Vaccination alone ensures protection against a disease.	False Antibody will take some time to develop (if disease has a short incubation period, it is worrisome).
	What post-exposure control would you want to use for a disease with- Short incubation period (ex: Tetanus) Long incubation period (ex: Hep B)	Short- passive immunization with specific immunoglobulin/antitoxin Long- combined active/passive immunization
	At what age does maternal antibody decay? Is it an example of active of passive immunity?	6 months Passive immunity (transplacental transfer and breast feeding)
	What specific equine antitoxins do we have available?	Diphtheria Botulism (type A, B, E)
	What is the definition of monoclonal antibody? Give an example of a monoclonal antibody used in clinical medicine today.	An antibody derived from a single type or clone of B cells (all the antibodies look the same) Ex: Palivizumab used in RSV prevention in premature children or infants with heart disease
	What are different classifications of viruses based on the preparation of their antigens?	- Live attenuated (virus or bacteria) - Inactivated (either whole or fractional)
	What is the advantage of a conjugate vaccine? Give an example of a vaccine that is commonly used and is conjugated.	Polysaccharide protein hooked to a protein. It is able to be processed by T cells so elicits Cell Mediated + Antibody immune response. ALSO Kids <2 yrs don't have B cell response towards pure Polysaccharides, so they need conjugate vaccine. H. flu aka Hemophilus Influenza (used to be the most common cause of bacterial meningitis), meningococcal, pneumococcal
	What are the advantages and disadvantages of live attenuated vaccines? Give some examples of live attenuated vaccines.	Advantage= typically one dose is effective; generates Cell mediated as well as humoral immunity Disadvantage= can cause severe rxn (ex Polio vaccine), unstable (must be kept at appropriate temp, etc.) ex: MMRV, Oral Polio (Sabin), Influenza, BCG, oral typhoid
	What are some examples of inactivated vaccines? What is the advantage/disadvantage of innactivated vaccines?	Whole cell: Killed Polio (Salk), Hep A, Pertussis Fractional: DPT, HPV, Influenza Advantage= not as much risk of adverse reactions Disadvantage= more humoral response, requires 3-5 doses, antibody titer diminish with age, not as effective as live (no mucosal immunity)
	By what age should you have all of your major vaccinations? What vaccinations are critical to administer at 2mo. of age and why?	Age 18 Pneumococcal and Meningococcal, common in young kids and we don't want them to be in danger when transplacental immunity wears off at age 6o.
	What is the difference between Adverse Reactions and Adverse Events?	Adverse reaction= side effect caused by vaccine, unintended effect (ex: pain, swelling, headache, allergic type response etc.) Adverse event= any event following vaccination, can be coincidental (ex: autism outbreak after MMR vaccine)
	What is a "contraindication" vs. a "precaution" as it applies to vaccination?	Contraindication= condition in a person receiving vaccination that greatly increases chance of adverse rxn. (ex: if someone has an egg allergy, don't give the the Flu vaccine that is cultured in eggs) Precaution= condition in a person receiving vaccination that can compromise the vaccine's ability to produce immunity OR in which it MAY cause an adverse reaction
	T or F As disease rates decline due to vaccination success, there is increase attention to the risks of vaccination.	True! We must instill public confidence in vaccine safety! It is important for community immunity! We have to continue monitoring for the safety.
	What are the three important phases of Prelicensure clinical trials for vaccines?	I- test new drug in small group, determine dosage and SIDE EFFECTS II- test drug in larger group to study EFFECTIVENESS and further evaluate SAFETY III- give to large group to confirm EFFECTIVENESS (Placebo and drug groups)
	What is the role of the VAERS (Vaccine Adverse Event Reporting system)?	It allows people to anonymously report adverse events. It attempts to detect potential risk factors.
	Which of the following are the major barriers to child immunization? A. low public awareness B. inadequate access to services C. missed opportunities to administter vaccine D. inadequate resources for prevention program E. all of the above	E. All of the above *300 children and ~42,000 adults in the US still die from vaccine preventable diseases
	Why are cases of neonatal tetanus uncommon in the US? Why is it that you have to get tetanus boosters every 10 years?	Most mother's have been vaccinated so children get passive immunity. Tetanus vaccine is made from Inactivated toxin, thus it will require boosters because Ab titers go down after some time.
	Why do adults get Tdap vaccinations (Td and p for Diphtheria and Pertussis) that traditionally have a lower dose of antigen than the DTP vaccines given to kids?	Because adults produce more severe immune responses to the antigen. The little d and the little p are used to indicate decreased dose of antigen.
	What is the causative agent of Pertussis? What is the difference between DTP and DTaP vaccine?	Bordatella pertussis (causes whooping cough, highly contagious) DTP = includes inactivated WHOLE CELL B. pertussis DTaP= includes inactivated PURIFIED ANTIGENS of B. pertussis used in US basically DTaP is similar to DTP but reduces rates of local and febrile rxns.
	Why was the administration of OPV (oral polio vaccine) discontinued in the US?	Live (Sabin) vaccination had adverse side effect in few cases (occurrence of VAPP- vaccine associated paralytic poliomyelitis). Replaced by IPV (salk)
	What are the two types of Pneumococcal vaccines?	Purified CPS (Capsular polysaccharide)- protect against 85-95% of invasive infections Protein-CPS conjugate- immunogenic in infants, protects against less serotypes (prevents 60% of infection)
	What is the most common cause of death due to infectious diseases?	Pneumonia *Along with Influenza, it is also the 5th leading cause of death in US
	What are the major anatomical barrier that protect a host against pnemonia?	1. Nasal hairs 2. Nasal turbinates 3. Sharp right angle bend (in throat)- bacteria can be taken up into lymphatics and eradicated
	Give an example of "normal flora" in the buccal cells? What happens when a patient becomes sick?	Normal= viridian strep Sick= proteolytic enzymes build up and clear the receptors so normal flora can get replaced by potential pathogens
	What is the "mucociliary elevator"? What conditions might inhibit this mechanism?	Helps purge the bacteria in the lower respiratory tract. The mucous traps the bacteria and the cilia help clear it out Change of mucus viscosity (ex: dehydration or electrolyte imbalance) Anesthetics and barbiturates impair cilia
	What is the role of Alveolar macrophages in the lower respiratory tract?	- 1st line of defense- kill intracellular organisms - APCs (present to T-cell) - source of cytokines, cause inflammatory response
	What are the 3 major routes of spread of pathogens that can affect the lower respiratory tract? Provide an example of a common bacteria that uses that route.	1. Aspiration of oropharyngeal secretions (strep pneumoneae) 2. Inhalation of aerosolized droplet (M. tuberculosis) 3. Hematogenous spread (Staph aureus)
	How many feet within an infected person do you have to be in order to catch an airborne pathogen (i.e. aerosolized in coughed secretions)?	within 3 feet usually Any further and rapid dehydration causes the fluid particles to become "droplet nuclei" and concentrate into dust.
	What is the most common route by which pathogens reach the lung?	Aspiration of contaminated oropharyngeal secretions (you can aspirate during sleep)
	What is the leading cause of community-acquired pneumonia? What does it look like on a sputum sample?	Streptococcus pneumoniae aka. pneumococcus gram + diplococci
	What does strep pneumoniae classically cause? Does it destroy the alveoli?	Lobar pneumonia Does NOT destroy alveolar walls. The alveoli are simply filled with polys and inflammatory cells making gas exchange difficult.
	What does H. influenzae look like? What demographic does it typically infect?	Very small Gram- cocci (can be pleomorphic) Salmon pink color Tend to affect young kids, smokers and those with underlying lung disease (emphysema)
	Which Gram - rods can cause pneumonia?	Klebsiella pneumoniae, Pseudomonas aeruginosa, E. coli * can cause necrotizing pneumonia, destruction of normal architecture
	What is the leading cause of pneumonia in infancy and early childhood? What does it look like in a sputum sample?	Staphylococcus aureus Gram + clusters ("grapes of wrath") Can cause necrotizing, abscess forming pneumonia (high mortality). Pus in lung= empyema
	What are the three atypical bacteria that can cause pneumonia?	Legionella pneumophila (water supply, immunosuppressed) Mycoplasma pneumoniae ("walking pneumonia") Chlamydaphilia species (psittacosis- from birds)
	What are the major clinical features that occur with Pneumonia?	1. Infection (fever, chill, malaise. Leukocytosis with left shift) 2. Respiratory tract irritation (cough, purulent sputum, hemoptysis- blood sputum) 3. Parenchymal inflamation (respiratory distress, pleuritic chest pain)
	What are some physical exam signs you might note in a patient with pneumonia?	- Rales/ crackles. popping sounds - Pleural rubs - evidence of consolidation
	What is "consolidation' and how can you tell if it exists on a physical exam?	Consolidation= fluid filled alveoli (lung becomes somewhat firm or consolidated) - dullness to percussion (no air) - inreased fremitus (vibrations heard), whispered pectoriloquy (sounds will have hollow quality to them, E --> A change = when they say E, you hear A)
	What will the radiographic appearance of Alveolar infiltrate look like?	BASICALLY: Alveoli filled with exudate but bronchi are spared - "ground glass appearance" of infiltrate - air bronchograms (open airway stands out in contrast to fluid filled alveoli)
	What will the radiographic appearance of Interstitial pneumonia look like?	- inflammation is only in interstitium - summation of many linear densities -reticulo-nodular, net-like pattern *tends to happen in viral pneumonias
	When one or more lobes are involved with alveolar infiltrate AND there is evidence of consolidation on physical exam, what Pneumonia Syndrome is it? What is a likely causative organism?	Lobar pneumonia *pneumococcus
	When one or more segments of the lung is involved and you hear rales without consolidation, what Pneumonia Syndrome is it?	Bronchopneumonia
	There are different types of pneumonia (according to setting where they are found). Describe the following: - Community acquired pneumonia (CAP) - Healthcare acquired pneumonia (HCAP) - Ventilator Associated Pneumonia (VAP)	CAP= pneumonia develops in ambulatory setting HCAP= develops in hospital/ healthcare setting --> VAP= caused by endotracheal intubation, etc., typically resitstant organisms
	What is the most common complication that occurs in 30% of patients with pneumonia? How can you tell if the effusion is an empyema when aspirated?	Pleural effusions (fluid in the pleural spaces of lung, which have been infected. Infected effusion or empyema, may need to be drained/aspirate) Low pH, increased protein and LDH (lactate dehydrogenase)
	Abscess formation as a complication pneumonia suggests that what groups of bacteria might be involved?	Typically Gram- rods H. flu S. aureus Anaerobic organisms
	What workup is recommended for someone coming in with pneumonia like symptoms?	-Chest X-ray - Sputum culture, blood culture - Assess oxygen status *special tests: - Serological test - Rapid diagnostic (DNA probe, urinary antigen)
	How soon should antibiotics be given after presentation with bacterial pneumonia?	Give early (preferably within 4-6 hrs)
	What are the two vaccines available to prevent pneumonia and how are they different?	1) Pneumovax, polysaccharide vaccine from 23 different strains 2) conjugated vaccine, protein form is used to vaccinate children
	What is the second most common infection? What demographic is particularly affected?	Urinary Tract Infection (UTI) Women >> Men
	When are men typically affected with UTI's?	Extremes of life: neonates- congenital obstruction elderly- prostatic hypertrophy
	At what stages of life are women affected with UTIs?	1. school age- increased chance of reflux because of cysto-ureteral junction abnormality 2. sexually active years- "honeymoon cystitis" 3. pregnancy (pyelitis) Asymptomatic infections also common in late stage of life (mostly in nursing homes)
	Why is it that women are more commonly affected with UTIs than men?	Anatomically shorter urethra (ease of access to bladder).
	How do most uropathogens access the urinary tract? What other routes of spread can occur?	Mostly originate in GI. Colonize vagina. Can retrograde spread to bladder. Rarely, hematogenous infection of kidney can occur.
	What are some key host defenses against uropathogens?	- micturation force rids bacteria in bladder - prostatic secretions = antibacterial - adherence of bacteria to wall promote apoptosis - adherence induce IL-8 (leukocyte migration) - antibody and complement inhibited by urine
	What are some major risk factors for getting UTIs?	- obstruction (stone, congential abnormality) - neuromuscular issue (impaired bladder emptying) - genetics - sexual activity - elderly women *estrogen deficiency, incontinence, catheterization)
	Bacteria that cause UTIs have numerous virulence factors. What is the "O-antigen" and " K-antigen" of E coli?	O- part of cell wall, LPS. Produces inflammatory response- fever, pain, hypotension (antigen) K- capsular antigen- prevents phagocytosis
	What are the adhesins on E. coli? What structure on E. coli helps promote motility (thus travel against urine flow)?	Pili or fimbriae mediate attachment of bacteria to epithelial cells. Flagella- organelle propulsion
	What is the role of the following in the pathogenesis of E.coli: - urease - siderophores - hemolysin	Urease- breaks down ammonia in urine (useful for forming stones). Siderophores- iron scavenging molecules Hemolysin- may lyse polys
	What is the difference between Type I pili and P-pili? Which one is competitively inhibited by a component in cranberry juice?	Type I: adheres to bladder mucosa and initially colonizes urethral meatus. * inhibited by CRANBERRY JUICE P-pili: seen mainly in pyelonephritis ( bacteria cause upper urinary tract infection)
	How does the pili on uropathogens lead to inflammation?	They stimulate a potent inflammatory response after binding to TLR on host cell.
	In what population do we tend to see asymtomatic bacteruria (asymptomatic UTIs)? What therapy should you give them?	Elderly women, typically in nursing home. DO NOT TREAT! They could become resistant. Only treat if pregnant, high risk pt, or child.
	What does dysruia mean? What is the clinical presentation of cystitis?	Dysruia= pain upon urination Dysuria, increased frequency, suprapubic pain, NO FEVER!
	What would you find in a urine sample of someone with cystitis? What organisms are primarily implicated?	WBC (usually >10^5 colonies/ml) E.coli (70-80%)>> staph saprophyticus
	What antibiotics can be used to treat bladder infections? What used to be used in the past but is now not due to rising resistance?	1. Nitrofuranotin (low resistance, low collateral damage) 2. Fosfomycin ----------------- alt. Fluroquinolones (reserve for more serious infection) (TMP/SMX not used)
	What is pyelonephritis? When should you suspect it?	Infection of the kidneys Suspect if: - frequent relapses - childhood UTI - subacute (1 wk+ presentation)
	How do you treat subactue pyelonephritis?	Longer course 10-14 days (b/c/ of potential to relapse) - check urine culture 2 wks after therapy is over to confirm
	What type of syndrome do you suspect in a 30 y/o woman with acute dysuria, watery vaginal discharges, hx of new sexual partner and a mucopurulent cervix on exam? How would you treat it?	Chlamydia urethritis Treat with doxycycline (also treat partner)
	A patient comes in to the ER with fever, chills and pain when urinating. She has pain and tenderness over the flank. Urine exam reveals WBCs in the urine as well as casts. What condition do you suspect?	Cystitis + fever + pain in costovertebral angle/flank = Acute Pyelonephritis
	What do you treat acute pyelonephritis?	Serious treatment for serious illness 14 day course of many antibiotics Fluoroquinolone Aminoglycoside 3rd gen. cephalosporin
	What is the difference between reinfection and replase as it applies to recurrent urinary tract infections?	Reinfection: different infective organisms with each episode. Typically due to antibiotic-sensitive pathogens, and uncomplicated infections. Relapse: pt is never free of infection between symptomatic bouts. Typically complicated infections, more likely antibiotic-resistant.
	In a patient with recurrent UTIs, if you culture the urine between episodes and find no bacteria, what type of recurrent infection would you suspect (i.e. re-infection or relapse)?	Reinfection. New bacteria every time. Uncomplicated. Treat with Nitrofurantoin. * TMP/SMX prophylaxis should be used if three or more UTI/yr
	T or F Voiding after sex or taking an antibiotic after sex is an important means of preventing UTIs.	False! But taking antibiotics before sex is helpful.
	What therapy would you use for recurrent UTIs that are relapsing in nature?	Prolonged treatment, at least 14 days. Remove catheter or any foreign body that could cause infection. Treat underlying abnormality if possible (or manage underlying conditions). Use urinary antiseptics like methanamine rather than antibiotics
	A man with fever, pain in the back, and burning upon urination comes in. You do a prostate exam and feel a large, tender prostate. What condition does he have and what should you treat it with?	Acute prostatitis Treat with Ceftriaxone plus gentamicin.
	What is the "chandelier sign" and what condition does it indicate?	A swollen, tender prostate, when massage, produces intense pain that will send a patient jumping into the air (presumably high enough to hit a chandelier).
	What are the symptoms of chronic prostatitis?	- History of recurrent UTI - Vague, nonspecific pain. - Prostate palpation doesn't cause pain
	How do you diagnose chronic prostatitis?	4 glass test = Fractionated urine cultures with prostatic massage. Collect urine sample --> do prostatic massage --> collect another sample. # of organisms in prostatic secretion >> # from initial urine/midstream bladder
	What are most antibiotics not capable of penetrating the prostate? What is used to treat chronic prostatitis?	Cant get past tight junctions of epithelial cells. TMP/SMX or ciprofloxacin (treat for 30 days)
	What is the number one cause of hospital acquired infections? What is the appropriate treatment?	UTI almost always due to indwelling Foley catheters (urethral cath). *so common that it is "non re-embursable" by medicare! REMOVE THE INDWELLING HARDWARE
	When someone has symptoms of a UTI and you order a urine dipstick and culture, what are they looking for for confirmation?	Urine analysis and microscopy: Looking for WBC in the urine, clumps and casts. Urine culture: specific organisms,susceptibility testing * in general, these tests look for presence of leukocyte esterase which is made only by WBCs
	Why are imaging studies done in the context of UTIs?	When stone/ obstruction is suspected. - CT (ex: potential abscess) - Ultrasound - Echo (for stones) - IVP= intravenous Pyelogram (dye outlines urinary tract, look for obstruction)
	Inflammation of the brain parenchyma is called ______. Inflammation of the spinal cord is called _______. Inflammation of the brain parenchyma and meninges is called _______.	1. Encephalitis 2. Myelitis 3. Meningoencephalitis
	The blood brain barrier is composed of cells cemented with tight junctions. Why is this a good and bad thing?	Good= protects most bacteria and viruses from getting in Bad= prevents protective components of humoral and cell-mediated immunity from getting in - difficult for Abx to get in (highly protein bound abx don't go through)
	What is the most common route that meningitis-causing bacteria take? How is it that they get past the mucosa, epithelial cells, and submucosa and into the bloodstream?	Hematogenous (via blood stream) IgA protease (gets past mucosa), pili facilitate endocytosis (intracellular invasion), enzymes and collagenase help invade inercellularly
	If the BBB is made up of tight junctions, how is it that certain bacteria can get through and cause meningitis?	1.Paracellular entry where there is lack of tight junctions between endothelial cells (ex: choroid plexus). --> meningococcus 2. Direct infection of endothelial cells (virus, pneumococcus, h.flu)
	What organisms can take the "neural route" of entry into the brain?	Typically viruses - infect peripheral nerves (ex: rabies) - latent virus that infects ganglia (ex: HSV) - olfactory endings (ex: arbovirus, N. fowleri protozoa eeks!)
	Give some examples of contiguous spread and direct inoculation that might lead to meningitis.	- Sinusitis, otitis media (adjacent foci) - rupture of a brain abscess - foreign body (infected LP, ventricular shunt) - skull fracture, trauma
	Though the brain and CSF has no immunoglobulins and poor levels of complement, it has some immunological surveillance. Describe.	1. microglial cells: derived from monocytes 2. Virchow-Robin spaces (lymph-like system, sheaths surrounding blood vessels, contain macrophage and lymphocytes)
	Why do people with meningitis present with headache?	Increased permeability of BBB- - vasogenic edema (separation of tight junctions) - decreased blood flow to brain - increased intracranial pressure
	What are the main bacteria we think of that cause Septic Bacterial meningitis?	Streptococci (S. pneumoniae), Staphylococci, GNBs (gram neg. bacteria)
	What are the main infectious agents that can cause ASCEPTIC meningitis?	Asceptic= routine bacterial culture came back negative. - viral - mycobacteria - fungi - spirochetes
	What are some non-infectious etiologies of meningitis?	- Autoimmune - Drug induced (NSAID, TMP/SMX) - Neoplasm - Subarachnoid hemorrhage
	Community acquired meningitis tends to be age specific. What bacteria are suspected in the following age groups? Birth-3 mo 5-35 yrs >60 yrs	Early in life: group B strep, E.coli (from traveling through birth canal), Listeria (transplacental) 5-35 yrs= college age, worry about N. meningitidis and H. flu >60= other extreme of life, S. pneumoniae, Listeria (waning T cell immunity)
	Nosocomial meningitis is typically caused by what type of bacteria?	Gram negative bacilli (ex: enterobacter, Pseudomonas- likes to live on hospital equiptment) - Strep and Staph also implicated - non-coagulase staph may be involved
	Is a patient with acute meningitis more likely to have a viral or bacterial etiology? What symptoms might be present? What is the time course?	Viral > bacterial for acute presentation Quatrad: fever, H/A, photophobia, stiff neck (possibly also AMS, lethargy, vomiting, coma) time course: hours- days
	What are the possible etiologies of a person presenting with chronic/subacute meningitis?	- fluctuating sxs over weeks, months Etiology: - TB, syphilis, crypto - chronic viral infection (RARE)
	What is "meningismus"? What are two physical exam tests that can be done to check for meningitis?	Meningismus= stiff neck Brudzinski's neck sign push neck forward and knees will bend reflexively Kernig's sign= flexed knee elicits pain both hint at inflammed meninges causing pain
	If someone with headache, nausea, and fever comes in and has CNIII palsy (i.e. eye is drooping), what condition might you suspect and what is the prognosis?	Suspect meningitis with CNIII palsy Poor prognosis- indicates that increased pressure is causing brain to herniate through 3rd or 4th ventricle
	In the case of young babies, what symptoms might indicate meningitis? What classic finding is associated with meningococcemia or acute bacteremia facilitated by N. meningitidis?	Babies- LOW threshold! listless and irritable, drowsy, refusing food. Fever and meningismus may be absent. Rash (ulcerating) associated with meningococcemia
	What does an initial workup for a patient in which you suspect bacterial meningitis involve?	Blood culture, LP, THEN antibiotics
	When should someone undergo a CT prior to an LP if you are suspecting infectious cause?	History of CNS disease, immunocompromised, or age> 60 - also if neuro exam is abnormal (aka focal findings) - Children (30% will present with szs)
	You perform a fundascopic exam on a patient with suspected bacterial meningitis and note swelling of the optic disc or papilledema. Why should you be careful when doing an LP?	Papilledema = increased IC pressure. If you do an LP, rapid release of pressure could cause herniation of the brain.
	What CSF profile is classic for bacterial meningitis?	- high opening pressure - elevated WBC (polys) - increased protein - decrease glucose (due to altered cerebral metabolis, decreased glucose transport) - gram stain + for bacteria in most cases - CSF turbid appearance
	What CSF profile suggests viral or asceptic meningitis?	- normal opening pressure - CSF pleocytosis with lymphocytic predominance - normal protein - normal glucose - Positive PCR of DNA in most cases - gram stain is negative
	What are the most common etiologies of viral meningitis?	- Enterovirus (Coxsackie and Echo) - Arbovirus (west nile) - HSV
	What is Mollaret's Meningitis?	- RECURRENT benign lymphocytic meningitis (>3 episodes with fever and stiff neck followed by spontaneous resolution) - mostly caused by HSV-2 - Dx via PCR - Rx: acyclovir
	A patient in the ER has presented with fever, stiff neck, photophobia and headache. You are highly suspicious of meningitis and want to do an LP but you anticipate a delay in setup. The patient is rapidly becoming worse and starting to vomit. What do you do?	Start on Antibiotics ASAP...then do the LP when you can (vomiting because its possible the brain is starting to herniate)
	What are the actions of corticosteroids?	- inhibit cytokine production - attenuate effects of LPS - may decrease things like edema, increased ICP, altered cerebral blood flow, vasculitis and neuronal injury *varied results from studies
	Should you re-LP someone with Bacterial meningitis?	No (unless they don't respond clinically within 48 hrs) (if they are a neonate with a GNB infection, might re-LP to determine duration of antibiotics)
	What are some complications of bacterial meningitis? What sequelae might occur?	Seizures septic shock DIC Herniation Hydrocephalus - in people who recover, risk of ID (intellectual disability, deafness, handicap)
	What vaccinations are out there that might prevent incidence of meningitis?	H. flu vaccine (now conjugated so you can give it to infants >2mo) Meningococcus (recommended before high school, college, etc.) Strep Pneumoniae - typically infants >2 mo and adults who are >65 or at risk/ immunocompromised
	How might someone with encephalitis present?	- altered level of consciousness - lethargic - confused/ hallucinating - seizures *delirium
	For the following, determine if they are more likely to cause encephalitis or meningitis: HSV-1 HSV-2	HSV-1 more likely encephalitis HSV-2 more likely meningitis
	What fungi might you suspect in the differential for encephalitis?	Crypto, Histo, Cocci, Blasto
	The most common bacterial organisms that can cause Brain abscesses are...?	Streptococci (S. milleri, S. pneumoniae) Staphylococci GNB Anaerobes
	What clinical symptoms are associated with a bacterial abscess?	- Focal neuro findings - anything suggestive of space-occupying lesion - N/V/ Headache - papilledema
	How do you diagnose a brain abscess?	- CT/ MRI - needle aspiration with culture
	How is a brain abscess treated?	- Antimicrobial therapy - surgery with drainage or excision - FNA (fine needle aspiration)
	Is it possible for a bacterial abscess in the brain to respond to antibiotics alone?	Yes, if they are small abscesses <3-4 cm
	If a patient comes in with focal neurological findings suggestive of a brain abscess but also presents with acute meningismus and fever, what do you suspect happened?	There was a periventricular abscess that ruptured into the ventricles causing inflammation and pain in the meninges.
	What physical exam finding would indicate a severe loss of fluid and dehydration (complication of diarrhea) that could lead to death?	Loss of skin turgor aka. tenting of the skin
	Why are we so concerned about diarrhea in children <3yrs, especially seen in developing countries?	It has been shown to STUNT growth (due to lack of nutrition). In addition it becomes a significant ECONOMIC burden for society.
	What are the various routes by which enteric pathogens are transmitted?	They must all somehow end up in stomach (orally). - foodbourne - water contamination - person to person (especially pathogens with low infectious dose)
	How do the following factors enhance the virulence of enteric bacteria? - adhesins - motility - toxins	Adhesins: help bind to GI cell receptor Motility: resist peristalsis Toxins: Enterotoxini and Cytotoxin- cause diarrhea or dysentery
	How do the following factors enhance the virulence of enteric bacteria? - extracellular enzymes (mucinase, proteinase) - capsule - serum resistance	Extracellular enzymes: they help break through the mucosa and cause invasiveness Polysaccharide capsule: resistance to phagocytes Serum resistance: circumvent opsonization and complement activation
	What are the two types of toxins enteric bacteria may produce and how do they differ in terms of effect?	Enterotoxin: causes net secretion of H2O + electrolytes into lumen. Cause Diarrhea Cytotoxin: kills cell, can cause bloody diarrhea, dysentery
	What are some examples of host defenses against enteric infections?	Gastric acid (compromised in newborns, ppl on acid blocking drugs, ppl who lose the ability to make HCl) Resident microflora, physical barriers (mucous layer), peristalsis, etc.
	What are some non-specific luminal factors that host cells have which defend against enteric infections?	Lysozyme- protect against bacteria Lactoferrin- Fe sequestering protein Breast milk- important Antibody protection for infants
	What is meant by the "ID50" of a pathogen? What enteric pathogens have a high ID50? What pathogens have low ID50?	ID50= dose of an agent that will cause 50% of people to become ill Shigella, C.jejuni- most infectious! low ID50 Cholera, ETEC- high ID50, need a lot more to be contagious
	Someone comes into the clinic with acute nausea and vomiting shortly after eating a piece of food. What type of toxin do you think caused this? Provide an example.	Pre-formed toxin (consider whenever there's upper GI problems!) ex: S. aureus (secreted toxin in food).
	A person who has watery diarrhea, cramping and urgency (need to go), has likely been affected by what kind of toxin? Give an example.	Enterotoxin (causes net increase of water in lumen) Ex: cholera, ETEC
	A person comes the ER. They have fever, abdominal pain, and bloody diarrhea. What type of toxin do you think did this to them? Give an example.	Bloody= Cytotoxin Ex: Shigella (invasion and destruction of cells)
	T or F S. typhi (a member of the Salmonella family) predominately presents with diarrhea like the others in the family.	False! results in Typhoid fever- insidious presentation (weightloss, fever malaise). Can involve rose spot rash. Diarrhea may occurs in some but not all individuals. Bacteremia is primary feature! Penetration of mucosa lead to spreading of pathogen.
	What does STEC stand for? What was it's previous name?	Shiga toxin producing E. coli Original name was EHEC or Enterohemorrhagic E. Coli
	ETEC primary affects what group of individuals?	Typically children or Travellers (T for traveler!) *the more often you get ETEC, the more immunity you develop. That's why adults tend not to get it as much.
	What two toxins does ETEC produce and what is their role in it's pathogenesis?	LT- heat labile ST- heat stable They are injected into the cell and they cause either increase in cAMP or increase in cGMP. Both leading to water accumulation in the lumen.
	Why is Cholera toxin called the Poisoned doughnut? What type of toxin is it?	5B: 1A (5 binding groups look identical) The bacteria binds to cell via B subunit and injects toxin. It gets cleaved and A subunit binds to adenolate cyclase causing net accumulation of cAMP (this is in the case of heat labile toxin).
	How long does illness caused by ETEC last? What is the major risk in terms of this infection and what are some clinical signs that indicate this?	Lasts about 5 days (incubation period is longer, 5-15 days) Major risk= DEHYDRATION - sunken eyes, dry mucous membrane, mental dullness, tenting of skin
	What is the strain of E. coli that is most frequently recognized as a source for bloody diarrhea in the developing world and has a low infectious dose?	E. coli O157:H7 like Shigella, requires less that 100 organisms to be infectious!
	How does the Shiga toxin work? How is Shigella transmitted?	5B:1A (same poisoned doughnut type of look), binds to ribosome on host and shuts off protein synthesis Typically food bourne (beef, lettuce, etc.) but because of low infectious dose, can also be transmitted person-to-person or even in petting zoos
	A person comes in to the hospital with bloody diarrhea, abdominal cramping and pain. After 7 days she is looking increasingly pale and puffy (peripheral edema). Blood smear shows low RBCs and her creatinine is >1.3 (renal failure). What is your diagnosis?	HUC or Hemolytic Uremic Syndrome *devastating complication of STEC (occurs in ~15% of people infected with STEC)
	What is the HUD triad? Explain why each of the conditions occurs.	Acute renal failure, hemolytic anemia, thrombocytopenia Endothelial swelling causes lumen to narrow, mechanical hemolysis of RBCs leading to anemia. Decreased blood flow to kidney causes renal failure. Platelets aggregate to plug up damaged endothelium. Use up platelets thus thrombocytopenia.
	What is the number 1 pathogen causing foodborne disease in the US? What is the number 2 pathogen?	#1= norovirus #2= salmonella (nontyphoidal)
	T or F A person with STEC infection should be given Antibiotics ASAP!	False!!! DO NOT TREAT. The person can be at significant risk to develop HUS.
	Aside from Gastroenteritis, what are some other clinical syndromes that Salmonella can cause?	Enteric fever= S. typhi Focal suppurative (pus) infections (ex: meningitis, osteomyelitis, etc.) Non-infectious sequelae, ex: reactive arthritis
	What age group is particularly inflicted by C. jejuni infectoins and why?	20 year olds - young folk don't cook food as thoroughly - also there might be underlying immune explanation here
	What does C. difficile stain with on gram stain?	Gram positive, SPORE FORMING, anaerobe
	What two toxins are produced by C. difficile and what does each do?	Toxin A= enterotoxin (binds brush border of gut, causing watery diarrhea) Toxin B= cytotoxin, causes cell death, inflammation, debris, mucous, fibrin (pseudomembranous colitis)
	T or F C. dif is part of the normal flora of most individuals.	False actually only normal in 1-3 percent of people . However you can have asymptomatic carriage! - dangerous because can be acquired nosocomially
	Elderly lady in the hospital develops pneumonia. She takes antibiotics and later develops severe abdominal pain, bleeding, and cramping for which she had to undergo a colectomy. This is a classic presentation of.......	Clostridium difficile!
	A child is brought to the clinic in February. He is not feeling well and has been vomitting. He also has had several episodes of loose stools (watery but no blood). What is the most likely pathogen he has?	Virus- Rotavirus (aka "winter vomiting disease) Predominately in kids. Typically no fever.
	What type of virus is implicated in diarrheal outbreaks typically in schools, cruise ships, hospitals, etc?	Norovirus (causes explosive, watery diarrhea and vomiting) crusie ships now have tight regulations to prevent this!
	What is the primary treatment for acute diarrhea?	Oral rehydration therapy *also think about selective use of anti-infectives depending on pathogen. Also encourage transmission prevention (hand washing, bleach ,etc.)
	For what diarrhea causing pathogens is antibiotic treatment always indicated?	Vibrio cholerae (Cholera) Shigella Typhoid fever (S. typhi) Usually indicated also in elderly, immunocompromised, chronic disease/malignancy
	When is Antibiotic treatment for Diarrhea typically not indicated?	ETEC (traveller's diarrhea) C. jejuni E. coli O157:H7 (risk of HUS!!)
	T or F All enterically acquired pathogens will cause enteric syndromes (N/V/D)	False! Example of nondiarrheal disease from enterically acquired infection- Hepatitis, C. jejuni (causing Guillain Barre), Hookworm (anemia)
	What types of genetic disorders (aka modes of inheritance) cause Congenital/ Primary Immunodeficiency (PID)	- single gene defect; SNPs - mostly autosomal recessive - few X-linked disorders
	What was the condition that the "Boy in the bubble" had? What types of immune barriers are lost in this disease?	Severe Combined Immune Deficiency or SCID lose both B cell and T cell function (basically non existent adaptive immune response). Very susceptible to infection.
	What is the overall incidence of Primary Immune Deficiencies? What percentage of children investigated for PID actually have an immune deficiency?	overall = 1:2000 only 10% of kids worked up for PID actually have a disease (so many factors involved, it gets very complicated)
	What are the roles of the following 2 cytokines: IL-12 IFN-g	IL-12: secreted by DC/macrophage- critical in differentiating Th cells, also stimulates INF-g, TNF-a, and NK cells and cytotoxic T-cell (does everything basically) IFN-g: revs up macrophages (increases their free radical killing)
	The majority of Primary Immune Deficiencies are characterized by defects in what cell?	B cells 2nd most common= SCID (combined B cell T cell) 3rd= T cell 4th= phagocytes last= complement defects
	Why do congenital immune defects not tend to present till 6mo. of age?	Because maternal IgG is keeping child protected. IgG waning during 6mo-12mo range--start to see defects
	What is Burton's X-linked agammaglobulinemia characterized by?	- X-linked syndrome - onset 6-24 mo - low IgM (low immunoglobulin)
	What is X-linked hyperIgM syndrome characterized by and what defect is present?	- high IgM, low other immunoglobulins - mutation in CD40L on T cells (prevents class switching activation)
	What is the defect in Common Variable Immunodeficiency? What types of infections are people with IgA deficiency prone to?	Common variable= IgG deficiency. Note: most common immune deficiency presenting in adults or after 10yrs IgA- loss of mucosal immunity, body is vulnerable to anything that can colonize that area
	A young boy is brought to the office with a history of recurrent ear infections. His blood test shows that IgG2 is deficient. The tests are otherwise normal. What syndrome might he have?	IgG subclass deficiency (there are 4 total subtypes)
	A child has had 2 episodes of pneumonia in his life. After the first episode, he was given Pneumovax. You highly suspect a specific anti-polysaccharide deficiency. What is one way you can test to see if this is the case?	You can vaccinate the child and then look at titers (see what body is producing in response)
	What are the two typical types of bacterial infections that you see in Defects in B cells/ antibody production?	1. encapsulated bacteria (pneumo, Hib) 2. enteroviral, gastrointestinal, or systemic (think of anything that can get past mucosal immunity)
	The following presentaiton all hint to what sort of congential immune defect? - recurrent bacterial ear infection - chronic gastroenteritis and milk allergy - chronic meningoencephalitis - absence of thymic shadow	B cell defect
	How are humoral immunodeficiency's treated?	monthly IVIG (if pt. has low IgG or deficit in specific antibody production)
	Why is IVIG contraindicated in patients with isolated IgA deficiencies?	IVIG has trace amounts of IgA in it. Person might attack IgA if body perceives it as foreign (since they have an IgA deficiency)
	When someone has a cell mediated primary immunodeficiency and for instance, has abnormal or very low T cell counts, what pathogens do you have to worry about?	Of course bacterial but ALSO viral, fungal, or opportunistic (ex: mycobacterium)
	T or F Patient's with Combined Immunodeficiency syndrome should be given BCG for TB prophylaxis.	False! Do NOT give live vaccines since they are severely immunodeficient (abnormal humoral and cell mediated immunity)
	What is the genetic defect in patients with severe combined immunodeficiency?	SCID= in 50% there's an IL-2 receptor defect.
	In ataxia telangiectasia, what is the main problem?	Defect in DNA repair enzymes (this causes the ataxia, spider angiomas, and decrease IgA)
	When you see a boy with eczema and thrombocytopenia, what clinical syndrome should you immediately think of?	Wiskott-Aldrich syndrome
	A patient comes to you with thymic aplasia, low PTH, low Calcium and congenital heart defect. What gene do you suspect he has a mutation in? What developmental anomaly does he have?	DiGeorge 22q11 defect defect in development of 3rd and 4th branchial pouch
	A person with chronic eczema and multiple skin abscesses also has a DOCK8 mutation. What syndrome do they have?	Hyper IgE syndrome = Job Syndrome (Job's body was covered with boils by Satan) Increased IgE supposedly because of unopposed activation by IL-4. IL-12 is somehow abnormal and causes decrease in IFNg leading to poor poly function.
	Recurrent, severe, or unusual bacterial infections, like infection in a youngster with P. jirovecii points to what type of congenital immune deficiency?	Combined T and B cell defect
	What is the appropriate treatment for a patient with T cell or Combined immunodeficiency'?	- bone marrow transplantation - gene therapy - to prevent GVHD (graft v. host), irradiate blood products. Make sure CMV negative.
	What is the principal defect in chronic granulomatous disease (CGD)? What test can you do to diagnose it?	X-linked, or AR disease NADPH oxidase defect (can't effectively kill catalase + bacteria) patient forms granulomas Dx: DHR assay (old NBT test)
	What is the defect in Leukocte Adhesion Defect I (LAD)?	- CD18 on neutrophils defect - affects B integrins and leukocyte adhesion - no pus or neutrophilia - ex: delayed umbillical cord separation
	A patient with silvery colored hair and eyebrows and recurrent staph infections, most likely has what syndrome/defect?	Chediak-Higashi - inability to fuse phagosome and lysosome
	Explain why a patient with Absent IL-12 receptor will be prone to disseminated mycobacterial infections?	IL-12 is the cytokine that stimulates many different cell lines including CD8+ T cells, which respond to intracellular bacteria.
	Why does cyclic neutropenia often go missed? What type of presentation will these people have?	1. rare (1 in a million type syndrome) 2. since neutropenia occurs for only a few days at a time, you can easily draw labs on a day when it is normal. Patients often present with periodic fevers
	What sorts of diagnostic clues would indicate a Phagocytic defect?	* for all of these you need polys/ macrophages - poor wound healing - delayed umbillical cord separation - soft tissue abscess/ - gingivitis/ periodontal disease
	Infections with what types of pathogens would likely lead you to consider a phagocytic defect? Why?	Staph aureus, Serratia, Burkholderia, Nocardia, Aspergillus * USMLE: SPACE= Staph, Psuedomonas, Aspergillus, Candida, Enterobactereaciae Catalase positive microorganisms- able to break down oxygen free radicals so neutrophils won't fight them.
	How does one treat/manage phagocytic disorders (such as CGD, cyclic neutropenia, etc.)? What treatment is used in the case of the most severe disorders?	- Use gamma interferon aka IFN-g (CGD) - G-CSF (cyclic neutropenia) - antibiotics *most severe types: Stem Cell transplant
	What sorts of clinical clues would make you think of a Complement Defect in a patient?	- angioedema (face, hands, GI tract) - pyogenic bacterial infections *- recurrent disseminated Nisserial infections
	Typically what pattern of inheritance do Complement Deficiencies fall under? If someone has recurrent Nisserial infections, what part of their complement pathway is disturbed? What about if they have Strep pneumoniae?	Autosomal dominant Nisseria (C5-9, C3) S. pneumoniae (alternative pathway, capsulated foreign polysaccharide)
	What is the defect in Hereditary Angioedema and what does it look like?	C1 esterase inhibitior deficiency C1 inhibitor blocks the activation of C1 (thus classical complement pathway) as well as parts of fibrin and kinin clotting system. Deficiency in this enzyme results in activation of bradykinin (which has vasoactive components) and causes allergic type swelling response.
	Defective membrane attack complex (C5-C9) leads to what types of presentation?	Disseminated Neisseria infections and meningococcal meningitis (aka N. meningitidis)
	How does one manage complement deficiency?	- the key is to recognize it and the prophylactically treat- meningococcal and pneumococcal vaccines - perhaps also provide antibiotics
	A patient of yours has had recurrent infections with pneumococcus, meningococcus and E.coli. You take a look at his blood and note distinct dark blue stain within RBCs. What is the explanation for his recurrent infections?	Asplenia Howell-Jolly bodies are indicative of this. Also because he is getting infections by encapsulated organisms (which the spleen is important in clearing).
	What are some warning signs of primary immunodeficiency?	- 8+ infections in a year - recurrent abscesses - persistent thrush in mouth (it's normal in babies, worry about HIV) - FTT - famix hx of immunodeficiency
	Sinusitis and otitis media are likely caused by a deficiency in what? Persistent liver abscesses indicates what type of disorder?	Sinusitis/otitis = B cell Abscess= neutrophil, CGD
	What is an absolutely essential part of the history of a patient with suspected primary immunodeficiency?	Age at presentation! <6-12 mo= SCID, T cell deficiencies 1-5 yrs= Hypogammaglobulinemia, CGD older, >5= specific antibody deficiency, complement disorder, common variable immunodeficiency
	What are the most important initial exam/ lab tests that clinicians must do when suspecting primary immunodeficiency?	Hx, physical exam labs: CBC w/ dif, Immunoglobulin levels
	What test would you order if you suspected CGD in a patient with a history of recurrent bacterial abscesses?	1. DHR or Dihydrorhodamine (blood cells are stained with DHR, if normal free radicals are produced, then DHR will reduce to rhodamine) 2. NBT or Nitroblue tetrazolium (typically turns blue with free radical production but in CGD it does not)
	What type of defect correlates with the following infections: 1. pyogenic bacteria, extracellular bacteria, S. aureus 2. viruses, fungi, mycobacterium, protozoa 3. S. pneumoniae, H. influenza, N. meningitidis	1. neutrophils 2. T cell dysfunction 3. antibodies as a rule, humoral immunity protects against extracellular and encapsulated. CMI protects against intracellular and other pathogens virus, bacteria, cancer*
	What branch of the immune system is implicated in Graft Versus Host Disease (GVHD)?	CD8 T cells. Cell Mediated Immunity.
	What kinds of disease states might be involved in Secondary Immunodificiency?	any Acquired state: - chronic disease - cancer chemotherapy - bone transplant/ organ transplant - splenectomy/ drug induced
	What is the principle defect in patients with Diabetes Mellitus that contributes to immunodificient states?	Impaired CMI (cell mediated immunity). Specifically, impaired neutrophil chemotaxis. Think of diabetes as a vascular problem where cells cannot disperse as well throughout body. High levels of glucose "feed" the bacteria.
	What sorts of infections would you see in a diabetic patient with uncontrolled glucose?	end organ damage. bone (osteomyelitis), urinary tract (UTI), TB, gangrene, cellulitis, etc.
	A patient comes in with onchomycoses (fungal infection of foot) and several ulcers in the foot. In addition they are draining pus like fluid from the eye and there is black eschar in the nose. What do you suspect caused this problem. When you see that they have high glucose levels in the blood, what might this indicate?	Mucor (black eschar in nasal cavity) also fungal infection of toe. Diabetic neuropathy causes loss of sensation to feet so they can't feel it. Need to maintain good glucose control!!
	What defect in a patient with end stage renal disease who has missed several dialysis treatments would cause someone to be immunocompromised?	Defect= uremia build up is immunosuppressive Depressed PMN, T and B cell activity, NK cell (pretty much everything)
	What type of infections could a person with end stage renal disease get in the hospital?	Potentially infection from catheter (S. aureus)- causing sepsis
	Why are patients with cirrhosis immunocompromised? What infections can ensue?	Shrunken cirrhotic liver causes backup of blood in spleen (due to portal hypertension) leading to it's enlargement. The spleen becomes hypofuncitonal. Thus encapsulated bacteria can infect easily (spleen is important for clearing encapsulated organisms out).
	What is vibrio vulnificus?	A gram neg., curved rod shaped bacteria (family Vibrio of the vibrio cholera fame). It can cause a blistering dermatitis and extensive bullos hemorrhagic lesions in septic patients.
	Why do we worry about patients who have connective tissue diseases (lupus or rheumatoid arthritis) getting infections? what happens if they are on an anti-TNF monoclonal antibody?	These patients typically have autoimmune neutropenia. Sometimes on steroids leading to T cell dysfunction. If they are on TNF blockers then they have higher risk of TB, S. pneumonia- dangerous infections. So they should get vaccinated.
	What is the definition of neutropenia?	when Absolute Neutrophil Count (ANC) is <500 cells. Typically pts become neutropenic 1 wk after starting chemo. * remember WBC x (%polys + %bands). Bands = immature polys extruded from bone marrow
	What sorts of factors can infection arise from in a cancer patient? ex: chemo itself	Chemotherapy - breakdown of normal skin and mucosa (rapidly dividing cells) from chemo - obstruction of an area from tumor (prevents immune cells from getting in) - immune defects (hematologic/ blood malignancies)
	What pathogens are of concern in a neutrophilic patient. Which pathogens would you be most concerned about and want to address first?	First address gram - bacteria (ex: pseudomonas). Also consider antibiotic resistant organisms (ex= MRSA, VRE, C. dif) - fungal infections typically if people have been neutropenic for a while. Also consider viral (reactivation type, HSV, VZV, CMV, etc.)
	What is echtyma gangrenosum? how does it differ from erythema multiforme?	Both abnormal SKIN findings: Ecthyma gangrenosum is a result of bacteremia causing end vessel obstruction (you see ulcerated skin lesions). When you see this, worry about P. aeruginosa (leading to bacteremia) Erythema multiforme is caused by IgM deposition. Mycoplasma or certain drugs can cause this. Characterized by swelling and allergic type reaction.
	What is considered "fever" in a neutropenic patient? What would you treat a Febrile Neutropenic patient with?	>38 degrees or 101 F for more than 1 hr Monotherapy- 3rd or 4th gen. cephalosporin (antipseudomonal), or monobactam (imipenem) You can also combine B-lactam and aminoglycoside synergistic combo Vanco use is controversial... 5+ days without fever reduction = start anti-fungals
	Why is it that patients who have bone marrow transplants are prone to infections?	1. In order to get transplant they have to undergo chemo (destroy cancerous cells and make room for new bone marrow). Absence of polys, T cells, etc. 2. GVHD (can damage epithelial surfaces and make ideal ground for infection). 3. acquire pathogens while in hospital OR get reactivation of previous pathogens when immunosuppressed
	What is GVHD? What cell primarily mediates these reactions?	Graft versus host disease- the donor's graft recognize the recipients cells as foreign and attack. T cell mediated disease
	What skin manifestations might you see in someone with GVHD?	Sloughing of skin- seen on arms, legs, mouth. Also sloughing of GI tract which causes diarrhea.
	What are some reasons that a person with GVHD is more susceptible to infections?	1. They can harbor latent infections (HSV, CMV, EBV, etc) that can resurface if stem cells are maturing. 2. GVHD cause Tcell dysfunction (from attack to immune system) allowing other bacteria to take over. Also causes systemic affects that increase susceptibility to being infected. 3. Steroids can further T cell defects
	What are the three phases of bone marrow transplant called?	1. Pre-engraftment / Early period 2. Early post-engraftment/ Middle 3. Late post-engraftment/ Late
	When does the Early period of Bone marrow transplant take place? What is the defect that is noticed and what kind of infections ensue?	1-4 weeks before engraftment causes neutropenia and loss of phagocytosis --> 1. extracellular gram +, gram- bacteria 2. Can cause fungal infections if prolonged neutropenia 3. Also reactivation of HSV, VZV.
	When does the middle phase of bone marrow transplant take place? What defect is seen and what sorts of infections does it cause?	Neutrophil engraftment to 3 mo. Defect= impaired CMI and humoral immunity Infections: 1. CMV! classic reactivation 2. Pneumonia 3. invasive fungal infections (ex: disseminated candidiasis) 4. EBV (reactivation causes post transplant lymphoproliferative disorder- fever + collection of B cells)
	When does the late phase of bone marrow transplantation take place? What defects are seen and what sorts of infections does it cause?	3 mo post transplant to years Defect: humoral and macrophage dysfunction with chronic GVHD (so chronic t-cell dysfunction). Infection: Everything pretty much: VZV, encapsulated bacteria, invasive fungi, catheter related diseases, late CMV disease
	What does a disseminated VZV infection look like? What stage of bone marrow transplant would it occur in?	Non dermatomal distribution (i.e. it crosses the midline). Occurs in late stage of bone marrow transplant.
	Recipients of organ transplants develop infections because of two basic issues. What are they?	1. initial surgery (anastomotic site and wounds) 2. prolonged, high levels of immunosuppression (mainly cell mediated immunity)- to prevent rejection from organ
	Early infections with organ transplants typically involve what types of pathogens?	Early on antibody dysfunction and neutrophil dysfunction- extracellular bacteria, typically at site of transplant. Also latent virus reactivation (HSV > CMV > HHV6)
	What is the most common virus to reactivate after organ transplant or bone marrow transplant?	HSV because of the way it lives (in ganglia) and since it doesn't tend to like stress. It can easily replicate and move down ganglia if it senses any stress.
	In the middle period after solid organ transplant, what pathogen is the major problem? What type of pathogens like to affect people in this phase?	CMV is a major problem (severe system illness can result, affecting every organ- glomerulopathy, bronchiolitis, liver "vanishing bile duct", etc) Intracellular pathogens in general like to affect people. Middle period- think Maximum T cell deficiency!
	What type of late infections are people with chronic or excessive doses of immunosuppressive agents (post organ transplants) susceptible to?	1. Intracellular bacteria 2. Pneumococcus 3. Various fungi 4. warts and HPV (and squamous cell carcinoma) 5. viral infections, CMV 6. EBV, PTLD
	What are the major early threats of renal transplants? What antimicrobial meds are these patients placed on and why?	- bacterial pylonephritis and wound infections - CMV and EBV are threats. CMV can cause glomerulopathy. - BK virus (K for kidney) can also affect patients. TMP/SMX to prevent PCP (pneumocystis pneumonia), and UTIs
	What are the major infectious complications of liver transplants?	Peritonitis and abscess and cholangitis. - also invasive fungal infections. Hep B or C reactivation and vanishing bile duct syndrome
	What is Cholangitis? What is "vanishing bile duct syndrome" and what virus is it associated with?	Cholangitis = infection of the bile duct CMV is associated with vanishing bile duct syndrome. Injury to liver causes obliteration of bile duct (basically rejection of bile duct).
	In Heart transplants, what could be a potential source of early infection?	Sternal wound infection, mediastinitis (potential early issue). Worry about Toxoplasmosis in these patients!
	What virus is associated with poor outcomes in heart transplant patients (ex: atypical lymphocytes, leukopenia/thrombocytopenia, and pneumonia). It is also the virus that is aossicated with accelerated coronary atherosclerosis in cardiac allograft recipients.	CMV associated with poor outcomes.
	In patients who undergo lung transplants, what clinical syndrome are you most worried about? What prophylaxis should these patients be given?	Lung so worry about Bacterial pneumonia (Pseudomonas or GNR0- gram negative rods). Give prophylaxis for PCP (pneumocystis pneumonia)
	In the middle phase of lung transplants, a virus can cause bronchiolitis obliterans in the lung, mimicking rejection. What virus is this and how does it look in tissue?	CMV is the problem looks like owl eye inclusion bodies in the affected cells.
	What antimicrobial prophylaxis could you use to prevent PCP, toxo, listeria, and some encapsulated bacteria)? What would you use to prevent CMV (also HSV)?	PC, toxo, listeria, H.flu, etc--> TMP/SMX Ganciclovir- prevent CMV, HSV * also treat Candida, Aspergillus with antifungals
	What is the appropriate regiment related to vaccinating BMT (bone marrow transplant) patients?	In BMT pts. antibodies decline over 1-4 years. - Vaccinate with Hib and pneumococcal vaccine every year to 2 years (12-24 mo) - give IVIG as needed for specific antibody deficiency
	Why is the spleen so important in clearing encapsulated organisms?	Because it is important for eliminating pathogens that aren't opsonized. There are macrophages and primary immunoglobulins in the spleen that can kill these organisms.
	What is the immunization procedure for someone getting a scheduled splenectomy? What if the splenectomy is an urgent case. What do you do then?	If elective: immunize 14days prior to surgery If non elective: immunize 14 days post surgery *you can give antibiotic prophylaxis to children
	What types of patients are "functionally hyposplenic"?	patients with SLE (lupus) RA (rheumatoid arthrits) sickle cell hereditary spherocytosis Ulcerative Colitis
	T or F Patients with iron overload and Burn/malnutritioned patients are also considered immunocompromised.	True these patients either enhance bacterial growth or have defects in CMI due to systemic/ multifactorial defects.
	What are the 5 P's of the Sexual history?	1. Partners (gender, #, etc.) 2. Pregnancy prevention (birth control, etc.) 3. Protection from STI (condoms, etc.) 4. Practices (oral, anal, etc.) 5. Past hx of STI
	Are women or men more likely to get Chlamydia? What age group is it most prevalent in?	4x more likely in women than men Highest prevalence in <25 yrs old.
	What type of infections can Chlamydia cause in men? What about in women?	Men: mostly asymptomatic (50%), otherwise urethritis, epididymitis, proctitis Women: acute urethral syndrome (scarring and ectopic pregnancy), Bartholinitis, cervicitis, salpingitis, PID, infertility, hepatitis (if it gets into peritoneal cavity)
	What are some techniques that can be done to diagnose Chlamydia infections?	Culture Non culture= Nucleic Acid Amplification Test (NAAT), Non-Amplification Test, Serology
	What is the advantage of a bacterial culture for diagnosing Chlamydia infections? Should it be used for screening?	Historically gold standard (not anymore). Very specific but LACKS sensitivity. Not suitable for screening. Takes too long, very complicated.
	What is the NAAT test (nucleic acid amplification test)? What are limitations to this test?	Amplify and detect organism's genome (DNA, RNA). Much more SENSITIVE. Can only be used in certain sites (urethra, cervix, urine. NOT rectum/pharynx)
	What are some non-amplification tests that can be used for Chlamydia testing?	1. DFA (direct fluorescent antibody)- Detects bacteria w/ fluorescent antibody 2. EIA (enzyme immunoassay)- detects bacterial antigen with enzyme-labeled antibody 3. Nuclei Acid Hybridization- detects specific DNA/ RNA sequences (like NAAT but no amplification)
	What is the appropriate treatment for Chlamydia? Which is faster?	1. Azithromycin (single dose) or 2. Doxycycline (7 days) * can do "test of cure" repeat testing 3-4 wks after (not in pregnant women)
	What demographic has a higher incidence of N. gonorrheae? What are the clinical manifestations of this syndrome in Men? In Women?	37 fold higher in African Americans (risk of low SES, early onset of sexual activity, etc.) can cause similar infections to chlamydia: Men- urethritis, epididymitis, proctitis, DGI (disseminated gonoccoal infection) Women- REVERSE from chlamydia. 50% asymptomatic. acute urethral, cervicitis, salpingitis, conjunctivitis, perihepatitis, DGI
	What special medium do N. gonorrhea cultures have to be done on? What other test beside cultures can be done for diagnosis?	Thayer-Martin - NAAT (ex: PCR) - Non-amplified test (ex: DNA probe)
	What is the treatment for uncomplicated Gonorrhea? Why are quinolones no longer recommended for treatment?	Cefixime (3rd gen) Ceftriaxone (4th gen) N. gonorrhea has developed resistance to quinolones.
	What are some symptoms of Disseminated Gonococcal Infection? How is it treated?	Pustular skin lesions Inflammation of tendons/joints Septic arthritis (most common cause of this in ppl under 40) Hospitalize and give IV antibiotics
	What might you see on examination of the cervix in a woman or urethral discharge in males with Gonorrhea?	Mucopurulent cervicitis or mucopurulent urethral discharge (in men)
	What should you expect to see on gram stain in a person with Gonorrhea? Would this be diagnostic in female patients? why or why not?	Gram negative diplococci within neutrophil Diagnostic only in males. Females have many bacteria that are natural part of vaginal tract.
	What would a primary infection with Treponema pallidium look like?	Syphilis - most likely single, painless ulcer or chancre at infection site
	What would a secondary infection with treponema palladium look like? What is the time frame like for this infection to develop?	- usually weeks to months to develop -systemic illness: low grade fever, sore throat, headache, rash, mucocutaneous lesions (genitals, mouth), alopecia (~10%), mild hepatitis
	What is the definition of latent syphilis? What is early latent vs. late latent?	Positive serology in absence of symptoms - Early: infection <1 year duration - Late: infection >1 year duration
	What is tertiary syphilis?	Can be benign: 10-15 yrs post infection, granulomatous lesions called gumma form, not contagious Cardiovascular syphilis: aneurysm, aortic valve insufficiency. You can also get tabes dorsalis, general paresis, opthalmologic problems *uveitis)
	What sorts of symptoms does one see in neurosyphilis?	paresis, tabes dorsalis (posterior column defect- ataxia, areflexia, etc.). Argyll Robertson pupil (small irregular pupil, fails to react to light but can converge).
	When would you use a Darkfield examination (DFA) to test for Syphilis?	When there is a primary lesion or a chancre. The organism can be seen in the fluorescent light.
	What serologic tests are available for diagnosing Syphilis? Why do you have to do both test?	1st- non troponemal (veneral disease research lab test) if positive 2nd- troponemal (specific antibody test FTA-ABS and MHA-TP *must do both because troponemal can be positive if there's lifelong immunity. But non-troponemal measures NONspecific antibodies (good for screening)
	What is the best treatment for Syphilis? What about neurosyphilis?	Benzathine penicillin given IM Penicillin G IV (10-14 days)
	What is the Jarisch-Herxheimer reaction and following what treatment does it occur?	Follows treatment for Syphillis with Penicillin: headache, myalgia, fever within 24 hours of treatment. (self limited- no need to treat but may give antipyretics)
	What does the treponema pallidum look like on darkfield microscopy? Can it be seen on gram stain? What if we see it in the mouth, is this diagnostic?	It's a spirochete (spiral organism). Can't be seen on gram stain because it is too thin. Not diagnostic if seen in mouth because mouth normally has some treponemes.
	How soon do you want to followup a patient with syphilis after they have undergone treatment?	typically serological Repeat testing in 6-12 months. Should have fourfold decrease in titer!
	What virus is the most common cause of genital ulceration in the world? What might the clinical manifestations of an episode with this virus look like?	HSV 2 Fever, headache, malaise, myalgias that recedes within a couple days after onset of lesion. also pain, itching, dysuria, vaginal discharge. Symptoms localize
	How does one diagnose Genital Herpes?	- look for clinical signs and symptoms - isolate virus via DNA detection (PCR) or HSV antigen (EIA, FA)
	What is a chancroid? What are buboes?	Painful ulcers of genitals + perianal area. associated with buboes. buboes= swelling of lymph nodes
	What pathogen causes Chancroids and how can it be diagnosed?	Hemophilus ducreyi Dx via gram stain (gram negative bacillus), also PCR
	What clinical syndrome do you suspect in a patient with a chronic, granulomatous ulcer on his penis?	Granuloma Inguinale (Donovanosis)- starts as firm papule/nodule that later ulcerates
	how do you diagnose Granuloma Inguinale aka Donovanosis? What types of cells is the organism found within?	Tissue smear or a biopsy of the ulcerated lesion showing negative rods aka Donovan bodies. Found within large mononuclear cells
	Chlamydia group L1, L2, and L3 are responsible for causing what sexually transmitted infection? What sorts of test can you use to diagnose this?	Lymphogranuloma venereum (painful enlargement of lymph nodes in inguinal and perirectal area). Diagnosis= usual suspects- serological test, tissue culture, histology, PCR
	What strains of HPV are most commonly associated with genital warts (non cancer causing)? What types are the major oncogenic strains and what kind of cancer are they most typically associated with?	warts- 6, 11 carcinoma- 16,18 (cervical cancer)
	What does HPV typically present as? What age group is mostly affected?	HPV- mostly asymptomatic, see warts in the genital region in both men and women. Age 20-24, over 50% of college age women affected.
	How does one diagnose HPV?	Look for genital warts. Also do HPV testing (look for DNA of virus) and Pap smears in women.
	What is new FDA approved vaccine available for both women and men to protect against HPV? What strains of HPV does it help prevent	Gardasil- recommended for girls and boys 11-12 yrs of age. 6,11,18,18 (warts and cancerous strains) Helps prevent Cervical cancer, genital warts, and dysplastic lesions in women and girls. In men, prevents HPV.
	What is the normal bacteria of the vagina?	Lactobacillus= normal bacteria of vagina that causes low pH
	What is Bacterial vaginosis characterized by? How is the diagnosis made?	replacement of lactobacillus sp. with anaerobic bacteria- MOSTLY asymptomatic Dx: fishy odor, high pH, homogenous discharge, clue cells (seen on microscopy). whiff test- if you add KOH, vaginal area smells more fishy
	If you look at the cervix of a woman with bacterial vaginosis, what do you anticipate seeing?	Frothy, watery discharge from the cervix that has a fishy smell
	What are "Clue cells" associated with and how do they look under a microscope?	Epithelial cells that have been loaded with bacteria on surface (making the edges look blurry) *associated with Bacterial Vaginosis
	A patient comes to you. She has had a history of miscarriages and preterm deliveries. On exam you note a non-smelly, yellow green discharge. What might the pathogen causing this be? How would you treat it?	Trichomonas vaginalis (a protozoan) dx: wet mount and culture rx: metronidazole, tinidazole (make sure to treat sexual partner!)
	A patient comes to the clinic complaining of discharge from her vagina and some soreness. PMHx reveals that she had been treated for strep throat 2 weeks prior. On exam you note clumpy, whitish discharge. What do you suspect to see under a microscope? What is the appropriate treatment?	Candida albicans (cottage cheese like discharge- yeast infection post antibiotic use). Microscope- yeast and PSEUDOhyphae *note can also occur in diabetic pts with glucose out of control. Rx: azole drugs, nystatin, fluconazole
	What is PID or Pelvic Inflammatory Disease characterized by?	Inflammatory disorder of upper GU tract in females - endometritis, salpingitis, pelvic peritonitis, abscess
	What are some clinical criteria that lead to a diagnosis?	Minimum criteria- lower abdominal tenderness, cervical motion tenderness Additional- temp >101 F, abnormal cervical/vaginal discharge, infection with N. gonorrhea or chlamydia
	In a patient with Pelvic Inflammatory Disease, what might you see on a transvaginal ultrasound? What is the appropriate treatment for PID?	Thickened fluid filled tubes (bascially inflammation of the upper GU tract) Rx: typically Abx, supportive therapy/hospitalization. Surgery for removal abscess if needed.
	What are the two major classes of skin and soft tissue infections (SSTI)?	1. no tissue necrosis (superficial to fascia) 2. necrosis (subcutaneous tissues +/- fascia, may involves muscle, bone, vasculature
	As a whole, most superficial infections are comprised of what type of bacteria?	superficial- mostly Gram + (empiric therapy)
	What are the resident microflora of the skin? What bacteria can colonize humans (and under certain conditions prove to be particularly dangerous)?	Resident flora = staph epidermidis (dry), gram negatives (moist) Colonizers= S. aureus (oropharynx), S. pyogenes (rarely/ transiently normal skin flora), Gram neg. colonize chronically ill/ hospitalized/ trauma (ex: P. aeruginosa)
	What do the following enzymes of S. aureus do? 1. Catalase 2. Hyaluronidase 3. B lactamase 4. Lipase, nuclease	Catalase- prevent O2 radical damage Hyaluronidase- hydrolyzes hyaluronic acid in CT matrix B-lactamase- inhibit penicillins/ B lactams lipase, nuclease (break down lipid and nucleic acid)
	Briefly, what do each of the following toxins of S. aureus do? 1.alpha toxin 2. beta toxin 3. leukocidin (P-V) 4. exfoliative toxin 5. TSST-1 6 enterotoxins	1. alpha- membrane damaging 2. beta- membrane damaging (no whole) 3. leukocidin: forms pore in phagocyte membrane 4. SSSS toxin- cause sskin to slough off 5. TSST- causes Toxic Shock syndrome 6. Enterotoxin- resist HCL
	Briefly describe the role of the following toxins and enzymes produced by Strep: 1. pyrogenic exotoxin 2. hemolysins 3. Dnase, hyaluronidase, streptokinase	1. pyrogenic exotoxin= supergenic antigen that causes scarlet fever 2. hemolysins: break down lysosomal content (S, O) 3. break down DNA, hydrolyze hyaluronic acid in CT matrix. kinase- dissolve fibril clot
	What is impetigo characterized by? What organism(s) are involved?	- seen in young kids (transmit within families) - multiple vesiculo-pustular lesion and then crust over (honey colored) - S.pyogenes +/- S. aureus SUPERFICIAL infection. S. aureus exfoliative toxin causes bullous disease (larger lesions)
	What is folliculitis characterized by? What organism(s) are involved?	- benign infection of hair follicle - raised, painful lesion, papular - no B symptoms (constitutional) - S.aureus; Pseudomonas (hot tubs)
	Describe the difference between furuncles and Carbuncles? What organism(s) are implicated in this?	Both= boil/ painful nodule at base of hair follicle/ sebaceous gland Furuncle- smaller; more superficial abscess in subQ tissue Carbuncle- larger, deeper. central necrosis and B symptoms (fever, sweats) S. aureus
	What does cellulitis look like? Where on the body is it frequently seen and why?	Cardinal inflammation signs (rubor, dolor, calor, tumor. no well demarcated)- infection of dermis and subQ fat - S. aureus and B-hemolytic strep is most common cause Mostly extremities because more prone to trauma
	What is erysipelas? What is the most likely pathogen(s) that causes this condition?	Form of cellulitis that heavily invades cutaneous lymphatics. Constitutional sxs present. Indurated areas (margins raised and well demarcated). S. pyrogens >>> S. aureus
	What is Ascending lymphangitis and how does it typically present?	It is a form of cellulitis wich progresses and drains through the lymphatics. Patients will be very sick and you may notice a red streak on skin/extremities outlining lymphatic drainage.
	What organism/toxin duo cause Staphylococcal scalded skin syndrome? What does this condition look like?	S. aureus/ exfoliative toxin - wide spread, erythematous rash with desquamation/peeling of skin (looks like a 2nd degree burn)
	What organism produces TSST-1 (Toxic Shock Syndrome Toxin-1)? What does the associated syndrome look like?	S. aureus (or streptococci) - fever, shock (hypotension), sunburn like rash with desquamation. Can disseminate and also have GI criteria.
	A young woman who has recently undergone a cesarean section for the birth of her daughter comes in to you one day. She does not appear well and has had an episode of fainting in the shower. Her tongue has little seed like bumps on it and her skin appears to be peeling on her palms. What syndrome does she have?	Toxic Shock Syndrome (post- surgical) - she has strawberry tongue, desquamation, and shock (hypotensive episode in shower)
	A patient comes in with a lesion in his arm that is looking inflamed and swollen. A day ago, he was bitten by his friend's cat. What organism do you think is producing this infection?	Pasteurella multocida (gram negative superficial infection!!)
	In general is it better to get bitten by a dog, human, or cat? Why?	Best to get bitten by dog (they tend to rip). cats tend to bite (so wounds are closed and don't drain as well). Humans have the dirtiest mouth flora (Strep, S. aureus, anaerobes, etc.)
	How do you distinguish the black eschar lesion seen in cutaneous anthrax from the necrotic lesions seen in the bite of a loxosceles Spider (brown recluse)?	Anthrax- round, regular , heaped up wounds. NON-tender vs. Spider bite- very painful, irregular borders, necrotic centers.
	What does echtyma gangrenosum look like? What is the primary organism that it is associated with?	Round/ oval lesion with a halo of erythema around it. In the center it is necrotic/black because the organism invades blood vessels and causes infarcts. Associated with P. aeruginosa (gram negative)
	What are the cutaneous manifestations of meningococcemia?	Classic rash that is disseminated. Also gangrene of distal region (acrocyanotic finger tips, because temperature is slightly lower and vasculature is not that great).
	Drug rash, rash associated with DGI (disseminated gonococcal infection), measles, lyme disease, and VZV shingles rash are all skin manifestations of what types of illnesses.	Skin manifestations of Systemic illnesses.
	What are some clues that a patient might have NECROTIZING skin and soft tissue infections?	1. erythema, edema, grey coloration. 2. dishwater drainage (as opposed to creamy, pus like)- indicates neutrophil defect 3. local anesthesia (failed pinprick test)= damage to superfiical nerves Tachycardia, tachypnea, fever, and Mental status change
	What risk factors might predispose someone to getting Synergistic (necrotizing) cellulitis/gangrene?	This is cellulitis combined with necrotic gangrene. This can occur in patients who have diabetes, alcoholism, malignancies, trauma, any vascular disorder. - may initially appear as cellulitis and then become echymotic/necrotic
	What parts of the skin does necrotizing fascitis involve? What organism is primarily involved and what skin changes are noted?	Epidermis, dermis, and superficial fascia (might also involve muscle). -Group A strep pyrogenes- red to blue/grey change in color, hemorrhagic, crepitus (air), gangrene. May get compartment syndrome.
	What is the more modern medical term for a "gas gangrene" and what organism is implicated in this?	Myonecrosis. Gram + anaerobic cocci. Clostridium perfringens
	A patient is brought the ER. He has a purple black superficial blister over his lower leg and severe cellulitis. He is in intense pain. History reveals that he is a chronic alcoholic and has spent a lot of time swimming in the gulf of mexico seawater. What do you suspect he has	Necrotizing cellulitis caused by Vibrio vulnificus The hemorrhagic bullae may occur. Risk factor= underlying liver disease and immune suppression.
	In general, what type of therapy is used for: - superficial, mild infections (ex: impetigo) - carbuncles, abscesses - deep tissue infection/ necrosis	- Superficial= oral antibiotic/ topical therapy - carbuncles, abscess- drainage recommended - deep tissue infection- hospital, IV antibiotics, surgery (for debridement)
	What is a vector? Distinguish between a passive and active vector?	Invertebrate organism that transmits a micro-organism from one vertebrate species (animal reservoir) to another (human) Passive- just a carrier Active- plays a role in replication, life cycle of organism (anopheles mosquito- malaria)
	What are the three most important arthropod vectors in the US?	1. ticks 2. mosquitoes 3. fleas
	Where is Lyme Disease most prevalent in the U.S.? What time of year do cases arise?	- Northeast**, Midwest (minnesota, wisconsin), Pacific coast - Summer months (june, july mainly but APRIL-SEPT)
	What organism transmitted by what tick is responsible for Lyme disease? How does the organism look under darkfield examination?	Ixodes mosquito (different species in different parts, NE= ixodes scapularis) Borrelia burdorferi = spirochete organism with flagella (motile)
	How long is the life cycle of B. burgdorferi in Ixodes scapularis? Describe it.	1. LARVAE infected in the SUMMER when it feeds 2. It lies dormant and emerges as NYMPH the next SPRING when it feeds again 3. Feeds one more time in the FALL as an ADULT and then lays more eggs Life cycle is 2 years. It feeds 3 total times (once in each stage of life)
	What is the size of a nymph tick? Why is it more likely that people will get Lyme disease in NE than in Midwest if both areas are infested with ixodes ticks?	Infectious load is different. In NE, up to 60% of ticks have Borelia burgdorferi. In Midwest, only 1% have it.
	T or F Lyme disease is the most common vector bourne disease in the US?	True ~30,000 cases annually
	When a patient calls in to tell you that they found a tick on their kid, what kinds of things do you want to ask?	1. Size- tot assess stage and whether the tick engorged- swollen (i.e. had it taken a blood meal, in which case more likely to cause problems) 2. Duration of time it was attached- needs at least 24 hrs to feed (falls off after 36hrs)
	When a tick bites you, what three things does it inject with it's proboscis?	1. liquid cement (that's why it's hard to peel them off) 2. anticoagulant 3. local anesthetic
	Why is it important, when removing a tick, to use forceps and pull it out perpendicularly to skin so it's head comes out?	Head part contains the salivary glands where the organism lives and if body is removed, the organisms can still disperse.
	Lyme disease presentation can be divided into 3 stages. Describe the first clinical phase and what symptoms you might encounter.	Stage 1: Erythema Migrans (bullseye rash). begin as maculepapule and then expand. Hot but painless. Non cutaneous- if spirochetes cross BBB, meningitis like sxs. Also flu like syndrome- chills, malaise, low grade fever and migratory arthralgias
	Why does the rash seen in the first stage of Lyme disease look like a bullseye?	Organism gets into skin and moves centrifugally creating this spiraling pattern.
	What does Stage II of Lyme disease present with?	a. Nervous system- asceptic meningitis, bells palsy, radiculopathies b. Cardiac- myopericarditis, heart block (rare- but suspect if seen in young person) c. Eye involvement- conjunctivitis, optic neuropathy, etc.
	Stage III of Lyme disease presents with what clinical symptoms? When do Stage II and III typically occur (how long after bite)?	Stage III= frank arthritis (monoarticular, asymmetric arthritis of large joints) Neurologic involvement- mood swings, irritability, focal CNS lesion (encephalitis), fatigue Stage II- weeks-mo after Stage III- months after (hard to diagnose because much removed from summer months)
	A person with Lyme disease present with 3 rashes on different parts of her torso. She isolated a single tick but you should be worried that there were others that she missed?	No. typically one tick can cause spreading of organisms leading to multiple rashes.
	How is Lymes Disease diagnosed?	1st- ELISA (blood, serological test). good sensitivity, but lots of false positives. 2nd- if positive, do Western Blot (may help distinguish false positives)
	Why should an antibody test not be used as a test of cure for Lyme disease post-treatment?	Because antibodies will be positive for about 2 years post infection. It might not necessarily mean that they have disease.
	What is the drug of choice to treat Lyme Disease? If someone is bitten and within a day comes to see you with the engorged tick in tow, is there some way you could treat them to prevent Lyme disease?	Doxycycline (po for 2-3 wks) Amoxicilin also works (kids <8yrs) Prophylaxis: single dose of oral Doxy can reduce risk by 80-90%
	What preventative measures can children/adults take so that they don't get tick bites or Lyme disease?	1. clothing, tight and light (to help detect tick) 2. Insecticide (DEET skin + clothes, Permethrin only clothes) Also constant inspection, and appropriate tick removal.
	What are the three types of Human Ehrlichiosis and what vector are they transmitted by?	Transmitted by deer tick (ixodes) and Lone star tick (one white dot, looks like Texas flag) 1. Human Monocytic Ehrlichiosis (HME)- monocytes 2. Human Granulocytic (HGE)- affects neutrophils *note HGA or human granulocytic anaplasmosis = HGE
	What does Ehrlichiosis look like in a peripheral blood smear?	Little clusters of cocci (coccobacili) in organism (look like a raspberry (morulae)
	What is particularly dangerous about a ruptured morulae as it applies to Ehrlichiosis?	1. It can disseminate in the blood stream (cause spread out effects) 2. Mosquitoes can take a blood meal and suck up bacteria which they transmit to others
	What doe Ehrlichiosis typically present with? What would you expect to find in their blood labs?	1. fever, headache, chills, myalgias 2. rash in only a minority labs- leukopenia (often with left shift), thrombocytopenia, anemia, etc.
	What age group is Ehrlichiosis particularly dangerous in? Where in the body is the tissue burden of HME and HGA the heaviest?	liver, spleen ,bone marrow, lymph nodes *typically worst presentation in elderly and babies.
	What are the two general of the family of organisms that causes Ehrlichiosis?	Family= Anaplasmatacea 1. Ehrlichia 2. Anaplasma
	What 3 tests can be done to diagnose Ehrilchiosis? What is the drug of choice for adults (and kids!) to treat this condition?	1. Serology, PCR, and blood smear 2. Doxycycline (for 10 days, oral) *typically don't like giving kids Doxy but exception b/c prevention of serious disease
	What type of infectious micro-organism causes Babesiosis? How is it transmitted to humans?	Intra-erythrocytic protozoan (Babesia microti) Ixodes scapularis tick
	What is the reservoir of Babesiosis? What are the MOST COMMON symptos of this condition?	White footed mouse mostly asymptomatic, but symptoms can be mild (myalgia, malaise, fever, H/A etc).
	What are the most severe symptoms of Babesiosis? What types of patients are particularly susceptible to these conditions?	jaundice, Disseminated intravascular coag (DIC), acute respiratory failure Splenectomy HIV/AIDS immunocompromised elderly
	What does the organism Babesia microti, look like on a giemsa stain (i.e. how can you distinguish it from malaria)?	Tetrad Merozoite (makes a Maltese cross symbol due to replicating within RBCs) *also distinguish from Malaria by taking a travel history
	Are blood transfusion treatments capable of killing Babesia protozoa? What treatment do you use?	No! several cases have been transferred via blood transfusion Mostly no need for treatment (self-recovery). In severe illness use Clindamycin and oral Quinine. *also exchange transfusions in some cases
	What is Rocky Mountain Spotted Fever caused by and what transmits this?	Rickettsia rickettsii Transmitted by dog tick (Dermacentor variabilis)
	What clinical findings are found in patients with RMSF (Rocky mountain spotted fever)?	few patients present with classic triad (fever, rash, hx of tick bite). Include macular rash spreading from ankles/wrists to trunk
	What is happening pathogenically in RMSF that produces the characteristic skin rash?	Rickettsia, after entering blood, invade endothelial cells- cause necrotizing small vessel vasculitis
	How would you diagnose someone for RMSF if they came in with a macular rash and fever?	1. PCR of blood 2. Biopsy of skin and look for organisms in endothelium
	What disease is caused by the Dermacentor andersoni? What does this tick produce that causes "Tick paralysis" syndrome?	Colorado tick fever (in Western coast) Produces a neurotoxin secreted in saliva or D. andersoni
	Coxiella can cause an aerosol trasmitted disease as well as a tick-bourne disease called...?	Q fever (considered a biothreat- category B
	What type of infection is Powassan viral encephalitis?	It is transmitted by a tick in Canada and northern New England.
	What causes Tularemia? What are the vectors for this conditino?	Gram negative bacillus (Francisella tularenis) vectors = dog tick, deer tick
	Why is Tularemia considered a weapon of bioterrorism? What syndromes does it cause?	Can be aerosoliezd and highly contagious (extreme biohazard) 1. ulceroglandular syndrome- cutaneous lesion with regional lymphadenitis 2. typhoidal- if ingested- fever, chills, weight loss 3. oculoglandular 4. pulmonary (inhalation)
	What is used to treat Tularemia?	Aminoglycosides, streptomycin, gentamicin.
	What organism causes the plague? Why is it called the "bubonic plague"?	Yersinia pestis (from a rat flea) You can develop these enlarged lymph nodes (bubos).
	How is the plague transmitted? Why is it a biothreat?	Transmitted by bloody, respiratory cough in addition to rat flea. It can cause pneumonic plague, septicemia, etc.
	How do you diagnose the plague? How do you treat it?	Diagnosed via gram stain (lymph node, sputum, blood) Treat via Aminoglycosides (streptomycin, gentamycin, etc.)
	How does Rickettsia typhi get spread from rat fleas or cat fleas? What syndrome does it cause?	Flea lands on you and when it bites, causes a pruritic rash. When you scratch it releases feces with the organism within. Causes Endemic Typhus (fever, headache, truncal rash- typically in homeless)

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Micro Id #2: Bacterial Diseases And Vaccination

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