Term
|
Definition
URT
-Cold.
-Viral: Rhinovirus & coronavirus
-cilliated epithelial cells of nose |
|
|
Term
|
Definition
URT
-Sore throat and tonsilitis
-Infected mucosa and lymphoid tissue
-Cytomegalovirus(CMV) blood to placenta
-EBV.
-S. pyogenes/N. gonorrhoeae/C. diptheria |
|
|
Term
| Otitis media and sinusitis |
|
Definition
URT
-Ear & sinus
-50% viral & 50% bacteria
-Respiratory syncytial virus (RSV)/Influenza/parainfluenza/rhinovirus/adenovirus
-S. pneumoniae/Haemophilus influenzae/Moraxella |
|
|
Term
|
Definition
URT
-H. influenzae type B(vaccine Hib)
-Ages 2-7
-Symptoms: Drooling/dysphagia/respiratory distress
-Life threatening if severe inflammation |
|
|
Term
|
Definition
LRT
-Virus:Parainfluenza(croup=barking seal)
RSV, Influenza, Adenovirus
-Bacteria: GAS, H. influenzae, S. Aureus
-C. diptheria(life threatening but vaccine-DaPT) |
|
|
Term
|
Definition
LRT
-Bordetella pertusis
-Attach to ciliated mucosa in trachea (fimbriae & hemagglutinin-prevents cilliary movement)
-Toxic factors:
1.Pertussis toxin-Prod mucoid secretions
2.Adenylate cyclase toxin-Inhibits chemotaxis,phagocytosis, & killing
3.Tracheal Cytotoxin-Kills tracheal epitherlia cells
4.Endotoxin
90-95% rate of infection if exposed to unvaccinated |
|
|
Term
|
Definition
LRT
-Inflammation of the tracheal/bronchial tree
-P. pathogens: Rhino corona, adeno, influenze viruses & Mycoplasma pneumoniae
-Secondary invaders-S. pneumoniae, H. influenzae |
|
|
Term
|
Definition
LRT-The flu
-Influenza virus types A, B, C,; A segmented RNA, 3 HA types, 2NA types
-Antigenic epitopes change from yr-yr(drift and shift)
-Airborne droplets |
|
|
Term
|
Definition
-Attaches via HA to sialic acid receptors on ciliated epithelium of trachea/bronchi
-RME |
|
|
Term
|
Definition
-Incubation 1-3 days
-Impair mucociliary clearance, tacheobronchitis, bronchospasms;cytokines released from damaged cells & WBC |
|
|
Term
| Presentation of Influenza |
|
Definition
-Fever of 102-104
-Chills
-Severe headache w/retro-orbital pain
-Muscular aches
-Dry cough
-Weakness
Resolves in 1-2 weeks |
|
|
Term
| Complications of Influenza |
|
Definition
Primary influenza-1% of cases but 30% fatal. Pregnant women at increased risk
Secondary Bacterial pneumonia-H. influenzae, S. pneumonia, S. aureus, S. pyogenes |
|
|
Term
| How many cases are required for influenza to be considered epidemic? |
|
Definition
|
|
Term
|
Definition
LRT
-Children <2
-Necrosis of epithelial cells lining bronchioles
-75% RSV (Respiratory Syncytial Virus)
Colonization:Nasopharynx-surface spikes are fusion proteins that fuse host cells to cause syncytia. Virus invades LRT by surface spread in secretions.
-Maternal Ab in infants react w/virus
-Presentaion:bluish ashy lips/cough/rapid respiration
-25% Other viruses |
|
|
Term
|
Definition
Respiratory Syncytial Virus
Paramyxovirus(RNA), enveloped
Humans only reservoir
Transmission:Resp. droplets to hands |
|
|
Term
|
Definition
LRT
-Pathogen clinically indistinguishable
Transmission: Inhalation of rep. droplets or aspration from UR
Colonization: Attach to rep. epithelium
Pathology: Respdistress from the interference of gas exchange in lungs,
Children: Viral maybe bacterial
Adults: Bacterial |
|
|
Term
|
Definition
Acute onset, high fever
Typicals: S. pneumoniae, H. influenzae, S. aureus, Klebsiella, E. coli, Pseudomonas
Atypical: M. pneumoniae, Chlamydia pneumoniae, Legionella pneumophila, Coxiella burnetii
-Chest Exam for: Rales(abnormal crackles)/Evidence of consolidation/Chest X-ray |
|
|
Term
|
Definition
Transmission: Inhaled or from blood
Colonization: Attach specifically
Orgs: RSV-Chlidren
Parainfluenza virus-Children; hemagglutinin & neuraminidase & fusion proteins
Adenovirus
Influenzavirus |
|
|
Term
|
Definition
Chronic
-Aspergaillus fumigatus: predisposing condition or immunosuppressed individuals. 45 degree branching septate hyphae present
-Histoplasma Capsulatum-Histoplasmosis
-Coccidiodes immitis-San Joaquin Valley Fever
-Blastomyces dermititidis-blastomycosis
-Pneumocystis jiroveci-pneumocystis pneumonia |
|
|
Term
|
Definition
Very Viscous bronchiol secretions leads to fluid stasis in the lungs & infections w/P. aeruginosa (S. auresus, H influenzae, B. cepacia
CF patients over reactive inflammatory response= too many PMNs, too much secretion=damage to mucosal epithelium, fluid stasis=bacteria are not removed |
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
| Steps for Infectous Microbes |
|
Definition
1. Entry
2. Spread
3. Multiplication
4. Evasion
5. Transmission
6. Pathology |
|
|
Term
| Gram Positive vs. Gram Negative Cell Wall |
|
Definition
GP: LTA
Thick peptidoglycan
resists activity of bile
Digested by lysozyme which targets beta 1-4 glycosidic linkages
GN: Thin peptidoglycan
LPS-Carbs: Stimulates immune response
Lipid A: Endotoxin that induces fever, ^vascular permeability |
|
|
Term
|
Definition
-Attach to a wide variety of surfaces
-More resistant to engulfment by host defense cells |
|
|
Term
|
Definition
-Movement
-Proteins are stongly antigenic/immune simulating |
|
|
Term
|
Definition
-aka common pili
-Attachment(adhesins target cell membranes) |
|
|
Term
|
Definition
| -Exchange genetic info, including antibiotic resistance |
|
|
Term
| Entry of bacteria into host |
|
Definition
-Direct contact
-Ingestion
-Fomites(inanimate objects) |
|
|
Term
| Clinical significance of normal microbiota |
|
Definition
-Common contaminants of clinical specimens
-Opportunistic pathogens |
|
|
Term
|
Definition
| Molecule that attaches to cells; providing a bridge to receptors on phagocytic cells and enhances the rate of phagocytosis |
|
|
Term
|
Definition
| Excess accumulation of serous fluid in connective tissue or in a serous cavity |
|
|
Term
|
Definition
| Abnormal redness of the skin due to capillary congestion (as in inflammation) |
|
|
Term
|
Definition
locall response to cellular injury
Marked by: Capillary dilation, leukocytic infiltration, redness, heat, pain, swelling, & often loss of function
-Serves as a mechanism initiating the elimination of noxious agents and damaged tissue |
|
|
Term
| Non-specific Physical Defenses |
|
Definition
-Overlapping epithelial cells
-Turbulence in nose that makes it hard for MOs to attach
-Shedding, scrapping, flushin(saliva, urine, tears)-Shear force
-Muco-ciliary clearance-goblet & ciliary cells |
|
|
Term
| Non-Specific Chemical Defenses |
|
Definition
1. Acids
2. Enzymes(lysozymes)
3.Microbiciidal chemicals (zinc & dermicidin) |
|
|
Term
| Non-Specific Biological Defenses |
|
Definition
1. Normal microbiota-Physical, competition, inhibitory substances
2. Immune defense cells and molecules |
|
|
Term
|
Definition
Inflammation
-phagocytic cells
-cytolytic cells
-acute phase proteins: CRP, interferon, and complement |
|
|
Term
| Signs of acute inflammation |
|
Definition
1. Erythema-redness
2. Edema-swelling
3. Heat
4. Pain (sensitivity to area) |
|
|
Term
| Triggers of accute inflammation |
|
Definition
1. IM
2. Peptidoglycan, LTA, LPS |
|
|
Term
|
Definition
-Engulf & destroy foreign matter
-Secrete chemicals (cytokines) |
|
|
Term
| Types of phagocytic cells |
|
Definition
-PMN=neutrophils
-mononuclear leukocytes |
|
|
Term
|
Definition
-Dominant in beginning of inflammatory response
-Contains cytoplasmic granules loaded with antimicrobial chemicals
-Best with extracellular pathogens |
|
|
Term
|
Definition
-Later in inflammatory response
-Concentrated in lung, liver, lymph nodes and spleen
-live longer than PMNs
-APC
-Best with intracelular pathogens |
|
|
Term
| Which type of phagocyte is best against extracellular pathogens? |
|
Definition
|
|
Term
| Microbe-PAMP to PRR-Phagocyte |
|
Definition
| Allows microbe and phagocyte to overcome negative-negative charge repulsion since both have exterior negative charges. |
|
|
Term
|
Definition
-Target viruses
-attach to infected to cells via glycoproteins
-release perforins & granzyme to kill cell |
|
|
Term
|
Definition
|
|
Term
|
Definition
Cytotoxic T cells
CD8
Kills cells infected w/intracellular pathogens |
|
|
Term
| Which MHC class do Th cells recognize? |
|
Definition
|
|
Term
| What MHC do Tc recognize? |
|
Definition
|
|
Term
| Activation of T lymphocytes |
|
Definition
1. Receive cytokines from APC(IL-1)
2. ^ of IL-2 Received adn secrete/receive Il-2=proliferation
3. Differentiation into: effector Th1 cells(activate macrophages=NK & Tc) & Th2 (activates B cells to make antibodies)
Memor Tcells |
|
|
Term
|
Definition
-Secreted by Th1
-Stimulates Tc proliferation & maturation |
|
|
Term
|
Definition
-Secreted by Th2
-Stimulates B cell proliferation & differentiation into plasma cells |
|
|
Term
|
Definition
-Secreted by Th1 cells
-Activates effector Tc, macrophages and NK to kill intracellular pathogens |
|
|
Term
|
Definition
|
|
Term
| What is a neutralizing antibody? |
|
Definition
|
|
Term
|
Definition
Delayed sequela of URT infection with group A beta-hemolytic strep
Abs that target strep bind to heart tissue due to similarity in receptors. IS cross reacts w/heart and kidneys |
|
|
Term
|
Definition
Caused by single base mutations in RNA. Slight changes in hemagglutinin (H) of influenza virus
Seasonal Epidemics |
|
|
Term
|
Definition
Major changes in surface proteins caused by recomvinationg of genes b/w 2 different strains of virus.
Pandemic |
|
|
Term
| What MO produce IgA protease? |
|
Definition
Nice STriP of Ham
Neisseria
Streptococcus pneumoniae
Haemophilus influenzae |
|
|
Term
| Which cytokines are responsible for fever? |
|
Definition
|
|
Term
| Physiological cause of fever |
|
Definition
| Hypothalamus secretes PG upon binding of IL-1 or TNF. PG then self activates the hypothalamus |
|
|
Term
|
Definition
|
|
Term
|
Definition
IgG
activated mins to hrs |
|
|
Term
|
Definition
Response to Ag-Ab complex
IgM & IgG stick to blood vessels or tissue activating C & neutrophils
Activated 3-8 hrs |
|
|
Term
| What type of hypersensitivity is the reaction to tuberculosis? |
|
Definition
Type 4
mediated by t-cells & macrophages |
|
|
Term
| Steps in a clinical encounter |
|
Definition
1. Patient History
2. Physical Examination
3. Investigation plan
4. Management plan |
|
|
Term
|
Definition
Upper Urinary Tract=kiney & ureter
Lower Urinary Tract= Urinary bladder & urethra |
|
|
Term
| Common community acquired UTI pathogens |
|
Definition
1. E. coli
2. S. Saprophyticus
3. Proteus miravilis
4. Klebsiella, Enterobacter, Serratia, Pseudomonas aeruginosa |
|
|
Term
| Hospital acquired UTI pathogens |
|
Definition
1. E. coli
2. Klebsiella, enterobacter, serratia, Pseudomonas aeurinosa
3. GPC
4. Proteus mirabilis |
|
|
Term
| Predisposing factors for UTI |
|
Definition
Anything that
Disrupts of urine flow
Preventscomplete emptying of bladder
Promotes microbial access |
|
|
Term
| Virulence factors of UTI E. coli |
|
Definition
O & K serotypes
-Pathogenicity island
-P fimbriae
-Capsular acid polysaccharid to resist phagocytosis
-Membran active cytotoxins |
|
|
Term
|
Definition
Adherence to uroepithelium
Microbistatic to GP & GN
Urease-ultimately increases pH cause stone formation allowing more attachment sites for pathogens |
|
|
Term
|
Definition
|
|
Term
|
Definition
LUT
-Dysuria(painful urination) |
|
|
Term
|
Definition
LUT Bladder
-Rapid onset of dysuria;^urgency/frequency
-Cloudy urine(pus or bacteria);blood |
|
|
Term
|
Definition
LUT Prostate
-dysuria, ^frequency, low back pain, fever |
|
|
Term
|
Definition
UUT Renal parencyma
-Cystitis+more sever FEVER
-Septicemia, loss of renal function |
|
|
Term
| How to collect urine samples |
|
Definition
Voiding(midstream)
Urinary catheter
Suprapubic bladder aspiration |
|
|
Term
| How do you distinguish cystitis from pyelonephritis? |
|
Definition
| Pyelonephritis includes sever fever |
|
|
Term
| What is consider clinically significant bacteriuria? |
|
Definition
|
|
Term
| What MO helps protect the vagina & how? |
|
Definition
| Lactobacili because it secretes acid=lower pH=barrier against infection |
|
|
Term
|
Definition
HumanPapillomavirus
Herpes Simplex Virus
HIV
Haemophilus ducreyi |
|
|
Term
|
Definition
HPV-Genital warts
-Attach via capsid protein, enter via RME
Pathology-Dyplasia(abnormal growth)
-Associated with cervical neoplasia |
|
|
Term
|
Definition
-Less cytoplasm=more sever dysplasia
-Mildly ^nuclear to cytoplasm ratio |
|
|
Term
|
Definition
Non-gonococcal urethritis
E-Abrasions
A-Receptors on host cell, parasite-induced endoytosis
S-asymptomatic or urethritis
C-infertility also PID, ectopic pregnancy
txt-tetracycline etc |
|
|
Term
|
Definition
Yeast infection
-Part of normal microbiota
T-disruptions to bacterial vagina community results in overgrowth with yeast
S-UTI, burning/cottage cheesy discharge
Balanitis(inflammation of glans penis)
txt-antifungal |
|
|
Term
|
Definition
Vaginitis-Protozoa
E-Vagina in women; Urethra/Prostate in men
S-Vaginitis, yellow/green frothy discharge. Rise in vaginal pH
txt-metranidazole |
|
|
Term
| Herpes Simplex Virus types 1 & 2 |
|
Definition
Genital Herpes
E-Membrane fusion
P-Causes host cells to fuse together forming giant cells.
S-Genital lesion vesicles->ulcer w/tender, swolen nodes, fever, headache, malaise
-Remains latent in root ganglion
-Can reactivate due to stress, trauma or sun |
|
|
Term
|
Definition
Gonorrhea
-Women have 20% chance of passing; Men 50-90%
E-Mucous membranes
A-Common pilus, Opa proteins. Invade non-ciliated e cells
P-LPS & Enzymes
-Neonatal blindness
TXT-Treat for gonorrhea (Cefixime & Ciprofloxacin) & Chlamydia |
|
|
Term
|
Definition
| Disease of immune cells-CD4(Macrophages & Th) |
|
|
Term
|
Definition
Syphilis
E-abrasions
S- Chancre 2-4 weeks postinfct
Primary-bacteria multiply in nodes causing swelling
Seconary- Bacteria multiply causing lesions. Most cured some become latent
Tertiary-Host cell-mediated response causes progressive destruction of neuro-, cardio-, skin, and joints
Txt-arsenic, penicillin, |
|
|
Term
|
Definition
-Inflammation of the stomach
-Pain in upper abdomen
-Bleeding |
|
|
Term
|
Definition
-Inflammation of stomach & intestines
-Diarrhea, nausea, vomiting, crampy abdominal pain |
|
|
Term
|
Definition
| Intestinal syndrome that primarily involves the colon or large intestines |
|
|
Term
|
Definition
| Inflammation of mucosa of both large & small intestine=dysentery-diarrhea often contains blood & mucus |
|
|
Term
|
Definition
Caused by liver damage
Patients become jaundiced due to bilirubin build up in the body |
|
|
Term
| How do pathogens cause disease in the GI tract? |
|
Definition
1) Action of toxins
2) Adherence to & effacement of microvilli=>inflammation
3) Invasion of intestinal epithelial cells |
|
|
Term
|
Definition
| Results in net secretion w/out intestinal damage |
|
|
Term
| Cytoskeleton-altering toxin |
|
Definition
| Alters cell shape, may injure cells but not lethal |
|
|
Term
|
Definition
| Causes cell damage and ultimately cell death |
|
|
Term
|
Definition
| Alters smooth muscle activity in intestines |
|
|
Term
| What causes bacterial food poining? |
|
Definition
| Ingesting preformed toxins; not infections |
|
|
Term
| Bacteria responsible for food poisoning |
|
Definition
Clostridium botulinum-botulism.
Staphylococcus aureus-most common. Starts 30 mins-8hrs post ingestion. Resolves in 24 hrs.
Bacillus cereus-Emetic. Starts 1-5hrs after ingestions. Lasts 1-6 hrs |
|
|
Term
| Pathology of Vibrio cholera |
|
Definition
S-Contaminate water
P-1. Ingest large numbers>10^8
2. Flagella allows Vibrio to reach epithelial cells
3. Attachment by way of fimbriae to receptors on brush border & crypt cells of small intestine
4. Damage due to production of CXT(A & B subunits). Disrupts adenylate cyclase. CXT=enterotoxin, neurotoxin, & cytotoxin
5.Secretion of large quatities of Cloride ion ino intestine. Water and sodium ion follow=hypersecretion of fluids & electrolytes |
|
|
Term
|
Definition
Extreme diarrhea, rice water stool
Dehydration & electrolyte imbalance=cardiac failure
Txt-Fluid & electrolyte replacement |
|
|
Term
| What mechanism do ETEC(Enterotoxigenic E. coli) and B. cereus use to cause disease? |
|
Definition
| Both colonize epithelial surfaces of small intestine & then release toxins. Do not enter cells. |
|
|
Term
| What mechanism does Shigella use to cause disease? |
|
Definition
| Atrach to and enter epithelial cells. Multiply intracellularly & destroy(efface) mirovilli of epithelial cells and induce diarrhea |
|
|
Term
|
Definition
S- Contact w/feces from infected person
P-1. descending infection of intestine. Small intestine then colon.
2. Capsule, secretes enterotoxin=watery diarrhea
3. Adhere to cells of colon using Outer membrane proteins
4. Use M cells of GALT and enterocytes to transport Shigella across intestinal epithelium using endocytosis.
5.Escape from phagolysosome
6. Triggers macs to produce IL-1 also triggers apoptosis
7. IL-1 induce inflammation & stimulates edema & extravasation of neutrophis across epithelial barrier
8. Movement of PMNs destroys barrier allowing shigella to move across in mass
9. Further prod. of cytokines & intense inflammation w/destruction of epithelium=>ulcerations=>blood in stool |
|
|
Term
| Symptoms of Shigella infection |
|
Definition
Blood and pus filled diarrhea
Self limiting 2-3 days |
|
|
Term
| What other baacteria share the disease mechanism of Shigella? |
|
Definition
EHEC
Yersinia enterocolitis
Entamoeba histolytic
Rotavirus/Norwalk virus |
|
|
Term
Salmonella enteritidis, S. typhmuium
Salmonella typhi, paratyphi |
|
Definition
Salmonellosis
Typhoid fever
Pathology:
1. Ingest lots of cells
2. Attach to fibronectin of epithelial cells of small intestine
3. Transported by M cells to GALT
4. Invade gut wall=ulcers adn hemorrhage. Spread to intestinal lymphatics & are phagocytized by macs
5. Produces toxin that ^cAMP & fluid secretion=loose, watery diarrhea & nausea
6. Causes influx of PMN that confines infection to GI
7. OR influx of macrophages which resuls in systemic spread. |
|
|
Term
| What mechanism do S. enteritidis & S. typhi use to cause disease in the GI? |
|
Definition
| Attaches, enters & multiplies in deep tissues that are normally sterile-submucosal or subepithelial tissues sometimes will spread systemically |
|
|
Term
| What mechanism do Hepatitis A virus, Reoviruses & Enteroviruses use to cause disease in the GI? |
|
Definition
| Attaches, enters & multiplies in deep tissues that are normally sterile-submucosal or subepithelial tissues sometimes will spread systemically |
|
|
Term
|
Definition
| High fever, headache, stiff neck |
|
|
Term
| How do MO get to the CNS? |
|
Definition
1. From the bloodstream-cross the BBB (Bacterial meningitis)
2. From peripheral nerves (Herpes, VZV, rabies)
3. Invasion from bone/sinuses/middle ear
4. Trauma |
|
|
Term
|
Definition
Acute febrile illness
Changes in mental state
consciousness
behavior |
|
|
Term
|
Definition
Acute-nearly always fatal
Neonates: E.coli, Group B strep
1mo to 5 yrs: Haemophilus influenzae type B
5 to 40 yrs: Neisseria meningitidis
30 and over:S. pneumoniae |
|
|
Term
|
Definition
Self-limiting/non-fatal
1. Enteroviruses
2. Arboviruses
3. HIV
4. HSV-2 |
|
|
Term
| CSF of bacterial meningitis vs viral |
|
Definition
Bacterial-elevated:neutrophils, protein. Decreased: glucose
Virus
Elevated:lymphocytes, protein.
Normal glucose |
|
|
Term
|
Definition
Very severe
1. Arboviruses
2. HSV-1
3. Eneroviruses, mumps
4. Rabies(Rhabodovirus) |
|
|
Term
|
Definition
Amebic encephalitis-Naegleria fowleri
African Sleeping Sickness-Trypanosoma |
|
|
Term
|
Definition
| Localized collection of pus |
|
|
Term
| Why are MOs in abscesses difficult to treat with antimicrobial agents? |
|
Definition
1. Microbes aren't multiplying
2. Chemical nature of pus interferes with action of some antibiotics
3. Hard to reach site due to lack of vessel penetrations |
|
|
Term
|
Definition
Strains of S. aureus with lysogenic phages
Causes splitting in deep layers=40% of outer skin layers are lost=loss of body fluid, high fever, and bacteremia |
|
|
Term
| Nectrotizing fasciitis/Flesh eating Strep |
|
Definition
GAS infected by phage
Subdermal tissues
2 toxins-Pyrogenic toxin A: superantigen-IL2
Exotoxin B-destroys tissues by breaking down protein 1in/hr |
|
|
Term
|
Definition
| Viral diseases resulting in skin rashes |
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
| Disease 5/Erythema infectiosum |
|
Definition
|
|
Term
| Diseae 6/Roseola infantum |
|
Definition
|
|
Term
| Most dangerous pathogen of burn damaged skin |
|
Definition
|
|
Term
| Sites of action of antimicrobials |
|
Definition
1. Cell wall synthesis
2. Cell membrane function
3. Nucleic acid synthesis or replication
4. Bacterial ribosome and protein synthesis
5. Metabolic pathways |
|
|
Term
|
Definition
Quinolline
DNA replication |
|
|
Term
|
Definition
Sulfonamide
Antimetabolites |
|
|
Term
|
Definition
Tetracyline
Protein synthesis |
|
|
Term
|
Definition
Aminoglycoside
Protein synthesis |
|
|
Term
|
Definition
Beta Lactam
cell wall synthesis |
|
|
