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Neisseria spp: Diplococci (aerobes), grows in a Thayer Martin agar (5% chocolate agar antibiotics for growth) and oxidase posititve. (gram negative bacteria) Use attachment pilus (OPA), Porin protein (POR) and lipoligosaccharide to affect organism Bacteria Strain Neisseria Gonorroheae Neisseria Meningitidis Disease Clinical Manifestations Gonorrhea Males: ureteral discharge and dysuria (usually colored thick pus) Females: cervical discharge and dysuria and severe pain. Meningoco Initially mild ccal pharyngitis, Meningitis sudden headache, fever, vomiting, stiff neck(CNS fluid build up) which can cause rash and then necrosis Mode of Transmission Sexual contact Risk Groups South east African America n 14-24 y Site of Infections Penis and vagina Mechanisms of Disease The damaged mucosa allows for a entry point and will replicate here and spread on this epithelia tissue into a bacteremia to the skin and to the joints. Contaminated respiratory droplets <5years CNS Coughed out and then breathed in and replicates in the nasopharyngeal epithelium and releases as a bacteremia to the lungs where you become infectious (in the lungs little replication) then you cough it out and that’s where it can affect the joints, CNS and heart. Gram Negative Bacteria coccobaccilus Bacteria Strain Disease Clinical Manifestations Catarhal (1-2 weeks): mucoid rhinorrhea, nasal congestion, sneezing Paroxysmal: intense bouts of coughs Convalescent: persistent cough Meningitis: pharyngitis (first symptom), headache, stiff neck, fever. Mode of transmi ssion Resp. droplets Risk groups Site of infectio n Lungs Mechanism of Disease Direct contact; contamin ated repertor y droplets Unvaccinat ed young children Lungs joints, brain, skin The bacteria colonize in the nasopharynx and will replicate in the lungs and the bacteremia will spread. Hib capsule (ribose, ribitol, phosphate PRP) and anti PRP response for clearance. *needs blood agar with hemin (x factor) and NAD. It goes into the mucosa or the skin where it will begin to replicate in these locations local macrophages and dendritic cells. Then will go into the lymph as a bacteremia and affect other tissues. It enters through the M cell and are directed to the ER and replicate there Enters through bite then replciates in Macs/CD usually doesn’t spread. Causes Macs to undergo apoptosis. Bordetella pertussis Whooping cough Schools homes Haemophilus (normal flora not encapsulated ) Influenza e Meningitis Epiglottiti s Celluaritis and Arthritis Brucella Spp Brucellosi s Acute (1-2wks): flu like Undulant (disease): fever, drenching sweats and other issues Through infected animals or contamin ated foods Farmers Liver, spleen, bone, heart Fracisella Tularensi s Tularemia UGD: fever, headache, chill, malaise, pain in involved areas (bites) lesion ulceratesnecrotic Ticks and rabbits Hunters in summer (tick) rabbit in winter Localize d at bite site It attaches to the lungs and replicates by FHA, P69 and PTX causing no ciliary action and increase cAMP. Cell debris + increase mucus +no ciliary action= cough Gram Positive anaerobes, faculatative or strictly anaerobic Bacteria Strain Disease Clinical Manifestation Mode of Risk Transmission group Site of infection Mechanism of Disease Actinomyces (facilitative, anaerobic) spp Actinomyc osis Endogenous spread teeth Teeth Form delicate filaments on the tooth and use gialdiase onto attach and invade on oral surfaces. Clostridium (anaerobe, mobile, spores) botulinum Botulism Clostridium (anaerobe, spores) flora difficile Pseudome mbranous colitis Boutulinum toxin A,B,E block neurotransmitters from binding and break cleave snare proteins which doesn’t allow acetylcholine to be released lack of muscle contraction Using A toxin to disrupt tight junctions and B toxin which is cytotoxic and its detected in the stool (ampicillin and clindamycin) Clostridium (anaerobe, motile, spores) Perfringens Gas gangrene or Clostridial food poisoning Chronic gramulomatous lesions, colonies of sulfur granules, infections mostly cervicofacial 18-36 hours: weakenss, dizziness, expressionless face progressive: nausea, vomiting, inability to swallow, loss of speech, respiratory paralysis Normal flora in % but when they go wrong it is in the hospital. Associated with antibiotics. Inflammation on mucosal surface Severe pain at woundedema discoloration stinky Incubation 8-24 nausea diarrhea (no fever) Spore ingestion from contaminated foods or direct contact Infants or foodborne Intestines and travels to CNS Spores Hospital Intestines Direct contact with spores (open wound) or ingestion (replicates in intestine/skin (deep tissue) Soil Open wounds intestines Enterotoxin attaches and increase Ca2+, theta toxin forms pores (heart) and alpha phospholipase dissolves cell membranes of RBC,WBC/muscle Gram positive (clostridium) Gram negative anaerobic bacteria (bacteriodes) weak to no gram stain Bacteria Strain Disease Clinical Mode of Risk Site of Manifestation Transmissio group infection n Clostridium (last gram positive) tetani Tetanus Bacteroides (gram negative, anaerobic, LPS w/o activity) fragilis Chlamydia (does not gram stain needs host ATP) Trachomatis Trachoma urogenital infection Legionella (Gimenez& Dieterle silver stain) Pneumophila Ligionnaires disease Early (4-5d)painful spasms then lockjaw. Progressive violent spams and respiratory causing death. Abscess formation causing intraabdominal infections Direct contact with spore into a wound People of soil Skin (endospore replicate and produce toxin) Via capsule binding on surfaces Sterile sites usually (wrong place at wrong time) Skin Follicular conjunctivitis, corneal scarring, blindness Urtheritis or cervictisi, dysuria, thin urethral discharge Fever, chills, headache, cough (75%) non productive Direct contact with contaminated secretions Inhalation of airborne microbes Epithelia of eye vagina or penis Travelers Lungs Mechanism of Disease Tetanospasmin binds & degrades synaptobrevin (docking site) which causes continuous muscle contract by blocking GABA and glycine release. Adhesions, short chain fatty acids (inhibit phag) enzymes (catalase, SOD tolerate o2, cytotoxic for tissue destruction). Toxin is heat labile zinc metalloprotease damages epithelium EB (metab inactive but infectious) enter host and prevent lysosome fusion. EBRB and these are meta active and will replicate and explode. Uses virulence (peptide toxin inhibits resp. burst, catalase and exotoxins) attacks Macs in summer. Bacteria Strain Disease Clinical Manifestation Mode of Risk Transmission group Site of infection Mechanism of Disease Mycobacteri um (aerobe, acid fast weak gram stain) Leprae (form tuberculoid Th1) Tuberculosis Th1 : granulomas primary tb (clinical) fever, night sweats etc or secondary 10% latent immunosup. Shows up again Contaminated respiratory droplets (viable for hours) People of soil Intracellular persistence it evades lysosome fusion and catabolizes NO and ROS. Activates macs IL1/TNF,IL12 forms granuloma Mycobacteri um Leprae (Th2 lepromatous) Respiratory droplets People Rickettsia Rickettsia (rocky mountain spotted fever) Rocky mountain spotted fever Tick bite Reservoir: dog/roden Skin Rickettsia (aerobic, gram – coccobacilli) prowazekii Epidemic typhus Erythematous macules, papules or nodules, extensive tissue destruction and foamy macrophages. Abrupt onset of fever, chills headache myalgia (2-12) rash from heads and to trunk Sudden fever, chills, headache, myaligai maculopapular rash (trunklimbs) Lungs reactivates in the CT, epithelial, muscle, nervous (bacteremi a) Skin/lungs Bite from louse the reservoir is humans Skin Ahderance by Omp A binding to endothelial cells then pathogenesis due to destruction of infected cells by bacteria. Ahderance by opma A binding to endothelial cells (destruction of cellsdisease) Inhibit TLR expression enhance phag, bacterial growth and instruct adapative humoral response (IL-4/IL-10) (weak cell response) Spirochetes Bacteria Strain Disease Clinical Manifestation Mode of Risk Transmission group Site of infection Mechanism of Disease Treponema (spirilla, gram -, cannot be gown in vitro) manifestatio n due to host inflame response. pallidum Syphilis Sexual contact, or congenital (in utero) Fetuses, sexually active Geneitals CNS Little Ag exposed (little response) outer membrane proteins have minimal expression and adhere to all body tissues and coated to avoid phagocytosis. Use hyalurodiase to break down cells Borrelia (Giemsa or Wright stain, large many flagella no either – or + burgdorferi Lyme Disease Primary: 2-6 wk incubation/dur. Painless 2 (6wk-6mo inc. 2 wk dur.): rash (trunk palms soles) flu Teritary (5-20 yrs) multiple orangs develop gummas, arteritis, menintgitis Erythema migransannular lesion with clear or necrotic center and raised red border, neurologic and cardiac symptoms, arthritis. Third ticks from mice/deer Humans Whole body Capable of antigen variation, antigenic modulation. The cell all contains a toxic LPS different form other bacteria endotoxin and the peptidoglycan has other inflammatory properties.