1. health and fitness
2. disease

Gram Positive Cocci: Strep and Staph Organism Staph Aureus Physiology/Structure Gram (+) cocci formed in clusters Facultative Anaerobes Catalase (+) Coagulase (+) Β‐Hemolytic Virulence A protein evades phagocytosis Coagulase forms fibrin clot around organism, protecting it from phagocytosis Toxic Shock Syndrome Toxin produces the superantigen TSST‐1 that leads to toxic shock. Exfoliatin causes the skin to slough off, disrupts desmosomes. Enterotoxin causes gastroenteritis Epidemiology Is normal flora found in mucous membranes and skin. Transmission can either be endogenous or exogenous. Common contamination is found in food workers that sneeze on their hands, then don’t wash. Found on food that has been left out, like potatoe salid. Enterrococcus (Fecalis and Fecium) Gram (+) Coccus, it is one of the Strep Species Lancefield Group D’ Can grown in Bile or in High Salt (6.5%) γ­Hemolytic PYR (+) Gram (+) Coccus Lancelfield Group A β­Hemolytic Bacitracin Sensitive to separate it from Strep Agalactiae Survives Bile and Salt so can colonize in the gall bladder. They are part of the normal flora of the GI and GU tract. During a procedure, they can be dislodged or displaced and presented to where they should no be. Normal Flora Most prevalent bacteria of GI tract Endogenous Transmission Theme is “escape or spread” M protein – antiphagocytic protein. M12 is associated with glomerular nephritis Streptolysin O – Oxygen Labile, antigenic cytolysin that causes lysis of cells. Streptolysin S – Oxygen Stabile, non­antigenic cytolysin that causes lysis of cells. “ASE”s Streptokinase, DNAase, Hyalurindase, all makes it easier to spread in tissue. Exotoxin A‐C that are superantigens and cause symptoms of scarlet fever Human throat, transmitted by aerosol droplets or endogenous infection. Sequellae of Disease (to fit better) Rheumatic Fever – possible sequella of untreated pharyngitis ONLY. This is a type II hypersensitivity reaction, where antibodies to the strep cross react with heart tissue. Causes endocartitis, a chorea, fever, and arthralgia. Poststreptococcal Glomerular Nephritis – possible sequella of untreated strep pharyngitis or skin infection. Type III hypersensitivity reaction. Immune complexes are deposited in the kidney, causing damage. Associated with M12 serotype Strep Pyogenes Diseases Gastroenteritis usually self limiting. Can be caused by ingestion of bacteria (then subsequent production of toxin) or by ingestion of heat stabile toxin produced before organism was killed by cooking. Scalded Skin Syndrome local infection produces a toxin distally. Causes mild epidermal tears, with a “sunburn like rash” Toxic Shock associated with tampons left in too long, toxin is a superantigen that causes fever, hypotension, and death Infective Endocarditis acute onset endocarditis with fever, malaise, and a heart murmur. Caused by cytolytic toxins UTI GI Æ GU Cholecystitis – infection of the gallbladder. Tx Gastroenteritis is self limiting, and the organism is passed with stool It is gram (+) with penicillinase activity, so Beta‐
Lactams don’t work. Methacillin and Nafcillin were drugs of choice because of their resistance to penicillinase. MRSA (methicillin resistant staph aureus) has made treatment more difficulty. Vancomycin is now the drug of choice, though resistant strains are being identified. Penicillin Pharyngitis – white, purulent lesions on the oropharynx. Scarlet fever – if strep throat is untreated it can then be accompanied by scarlet fever. It is described as a sand‐
paper rash, also called a sun burn‐like rash, in that the skin is red. The palms and soles are spared. There is also a strawberry tongue that presents bright red with many bumps. Impetigo ‐ just like staph aureus Necrotizing Fasciitis ‐ infection that causes “flesh‐eating bacteria.” Rapid spread through fascial layer can involve large amounts of tissue requiring debreidment or amputation. Culture all negatives on a rapid test. β­Lactams work well. In those with allergies, use macrolides. Organism Strep Pneumoniae Physiology/Structure Gram (+) Coccus Lancet­Shaped Diplococci No Lancelfield Group α­Hemolytic Optochin Sensitive to separate it from Viridans group Virulence Capsule – most important virulence factor IgA protease – cleaves IgA that allows colonization of mucosa. Pneumolysin O – what is responsible for the rust colored sputum associated with the disease. Destroys ciliated cells by inducing classic complement. Epidemiology Normal flora of the upper respiratory tract. They can be colonized, but not be infected. Any immunocompromise (chronic pulmonary disease, viral infection, spleen‐ectomy) can lead to pathogenesis Diseases Acute Pneumonia rapid onset of fever and chills, pain on inspiration, and an X‐
ray with infilitrates Otitis Media – most common cause of otitis media in children, despite vaccine. Sinusitus – same as otitis media, commonly causes sinusitis in kids Adult Meningitis – since the vaccine for H. Influenzae b (later), now is leading cause of meningitis in neonates. Viridans group Gram (+) Coccus No Lancelfield Group α­Hemolytic Optochin Resistant to separate it from S. Penuemo Dextran Bioslime that both protect the organism from the immune system and increases adherence to teeth or heart valves This is a variety of organisms such as S. Mutans. S. Mutans is part of the normal flora of dental caries. These buggers cause plaque. Plaque then allows other Viridans group to colonize and cause cavities Subacute Endocarditis – dental surgery gives S. Mutans access to the blood stream where it colonizes the mitral valve. This is why people with prostethic valves or previous valve problems get prophylactic antibiotics before dental procedures. Tx Macrolides for adult bacterial pneumonia Third Generation Cephalosporin for meningitis Vaccines are available. The pediatric vaccine covers 7 common serotypes protecting against meningitis. The adult vaccine covers 23 common serotypes to protect against pneumonia Penicillin often prophylactic for endocarditis. In pharm, you learn you treat with Clindamycin or a combination of Vancomycin + Gentamycin. Gram Positive Rods: BCC LAN LM “Send an Email (BCC) over the network (LAN) to Lincoln Martin (LM)” Bacillus, Corynebacterium, Clostridium, Lactobacillus, Actinomyces, Nocardia, Listeria, Mycobacteria; you know “N” is NOT neisseria because Mycobacteria and Nocardia are similar. Organism Bacillus Anthracis Physiology/Structure Gram (+) Rod Forms spores Is unique for its polypeptide capsule (most others are polysaccharide) Facultatively Anaerobic Bacillus Cereus Gram (+) Rod Forms spores Same as Bacillus Anthracis Corynebacterium Diphtheriae Gram (+) Rod Aerobic Non‐spore formers Form “Chinese Letters” on gram stain, V or L shape. Grow Grey or Black colonies on Tellurite Loeffler’s Media causes granule formation Virulence Spore Forming so they are highly resistant to drying, desiccation, heating, etc. Antiphagocytic Capsule evades phagocytosis Exotoxins Edema Factor – calmodulin dependent increase in cAMP leading to fluid extrusion. Lethal Factor – causes tissue necrosis. Protective Factor ‐allows entry of toxins into target cells. Called this because it is target of vaccine. Similar virulence to Anthracis, has different toxins Exotoxins Emetic Toxin causes N/V/D 1‐6 hrs after ingestion Diarrheal Toxin causes a cAMP dependent secretory diarrhea similar to Cholera or ETEC Toxin – inhibits protein synthesis. It is a classic AB toxin that inhibits EF‐
2 While it colonizes the naso or oropharynx, it is not invasive Epidemiology Found in soil, water, and on animals (particularly sheep). Can be inoculated into a cutaneous wound or inhaled into the lungs. Possible agent of bioterrorism (note the postal scare). Found on food that was cooked and reheated. Think buffet line at a Chinese food restaurant. The classic presentation is fried rice at a Chinese buffet. Throat and nasopharynx, usually transmitted by respiratory droplets. Diseases Cutaneous Anthrax is 95% of all anthrax cases. Spores get into wound causing black painless swollen postules called eschars. They crust over and resolve spontaneously. They can rarely enter circulation and cause fatal septicemia. Pulmonary Anthrax (Woolsorter’s Disease). Inhaled spores cause hemorrhagic lymphedemitis with mediastinal widening. It resembles many pulmonary diseases initially, and is rapidly fatal without treatement. Normally transmitted by sheep, it is now a risk of bioterrorism. Gastroenteritis­like symptoms Diphtheria – Grey pseudomembrane that is on the pharynx. It is well attached and will cause hemorrhage if removed. It is here that necrotic tissue, leukocytes, and the corynebacterium are. If the membrane gets to large, it can cause respiratory obstruction. Bull Neck – swelling of the neck out Diagnosis Formerly Penicillin (which may still work). Currently use doxycyline or cirpofloxain Self Limiting Elek test will confirm toxin producing strains. In this test, bacteria are streaked across a plate, with a elek strip placed across all streaks. It contains an anti‐toxin that causes precipitation Antitoxin is top priority to neutralize toxin Antibiotics will kill bacteria, and stop the toxin production DPT vaccine Organism Physiology/Structure Virulence Epidemiology Diseases Diagnosis Clostridium Tetani Same as other clostridium species, no double zone of hemolysis Tetanus Toxin (tetanospasmin)– causes spastic paralysis known as Tetanus. Classic AB toxin that targets the central nervous system, inhibiting inhibitory neurons by preventing vesicle transport and fusion. No fusion = no release. No release = disinhibition of skeletal muscles = contraction. Targets GABA and glycine. Found in dirt, soil, or dust. Common presentation is a penetrating wound (such as a rusty nail). Tetanus Bacteria colonize a local infection, housed in necrotic tissue (anaerobic space). Secrete exotoxin that travels everywhere, targets the CNS inhibitory neurons. Symptoms begin with trismus (lockjaw) and risus sardonic us (a smile that cannot be stopped) Progresses to a spastic paralysis with death resulting from spasm of diaphragm
Antitoxin binds and neutralizes free toxin in circulation Toxoid (aka the vaccine) conveys long term neutralization of toxin and active immunity. Survival DOES NOT convey immunity. Give injections at separate sites Muscle Relaxants (benzos) to alleviate contractions Clostridium Botulinum Same as other clostridium species, no double zone of hemolysis It is also found in dirt, soil, or dust, that can cause the low‐yield wound botulism. Found in home­canned foods that are not cooked well enough. Found in honey given to newborns. Adult Botulism – food contaminated with botulism is not cooked or prepared well enough. Begins with dipolia and dysphagia, progressing to flaccid paralysis and death from flaccid diaphragm Infant Botulism – honey contaminated with botulism in an infant less than one year old. Begins with constipation and feeding problems progressing to floppy baby syndrome. Palliative care to provide ventilator support Antitoxin to alleviate circulating toxin (any toxin in cells has already taken effect). Penicillin to kill bacteria Clostridium Difficle Same as other clostridium species, no double zone of hemolysis BotulismToxin – causes spastic paralysis known as Botulism. Classic AB toxin that targets the peripheral nerves, inhibiting NMJ neurons by preventing vesicle transport and fusion. No fusion = no release. No release = inhibition of skeletal muscles = flaccid. Targets ACh Toxin A = Enterotoxin Causes inflammation and secretory diarrhea Toxin B = Cytotoxin Disrupts protein synthesis and causes disorganization of the cytoskeleton. Part of the normal GI Flora. When on broad­spectrum antibiotics the normal flora is eliminated. This is highly resistant, so then grows in the space left by the previous flora. Psuedomembranous Colitis – watery, secretory diarrhea that results from the enterotoxin. Ulcerations can be visualized on endoscopy resulting from Cytotoxin. Cultures will be positive (normal flora), but a tox screen of stool will confirm diagnosis. Discontinue antibiotic therapy. Give oral vancomycin (one of the few drugs it is NOT resistant to). You must give it orally because vancomycin cannot penetrate GI barrier, and the infection is in the GI tract. Lactobacillus Low­yield organism Know that it maintains the vaginal pH to prevent exogenous infection. When giving broad‐spectrum antibiotics, you can kill lactobacillus, and allow overgrowth of other organisms (like candida) Actinomyces Israelii Facultatively anaerobic/strictly anaerobic NOT acidfast (contrast to Nocardia) Grow slowly Filamentous hyphae Resemble “grains of sand” ‐> sulfur granules NOT found on skin Colonize URT, GI, female genital tracts
Actinomycosis – chronic granulomatous lesions ‐> suppurative and form abscesses No person to person spread Disease from soil or water Cervicofacial infections ‐> poor oral hygiene; invasive dental procedure Thoracic infections ‐> Hx of aspiration ‐> spreads to lung‐adjoining tissues Abdominal infections ‐> GI surgery; trauma to bowel Pelvic infections ‐> secondary manifestation of abdominal actinomycosis; primary infection of woman with IUD CNS ‐> hematogenous spread from other tissues
Most cases: Cervico facial ‐> draining sinus tracts along angle of jaw/neck Difficult
Culturing is slow Sulfur granules ‐> tin, gram positive, branching rods around periphery Nocardia Asteroides Gram (+) branching rods. Partially Acid­Fast Aerobic Ill defined pathogenesis Reservoir is Soil and Dust, thus there is an exogenous inoculation via trauma or inhalation. (Inhalation) Cavitary Broncholpulmonary Nocardosis – often associated with immune compromised patients. Symptoms are fever, cough, diffuse pneumonia with cavitation of the lungs. Spread via the blood to the brain. (Traumatic Implantation) Subcutaneous nocardosis – training type of sinus tracts and granules. This is similar to actinomyces only with a traumatic implantation. Sulfonamides Listeria monocytogenes G+ve coccobacili ‐> arranged in pairs resembling enterococci Faculative anaerobes Motile at room temp, weakly β‐hemolytic, capable of growth at 4°C and high salt concentration Facultative intracellular pathogen that can avoid Ab‐mediated clearance Virulent Strains produce cell attachment factors (internallins), hemolysins (listeriolysin O, two phospholipase Cs), and a protein that mediates actin‐directed motility (ActA) “Actin rockets” – cell to cell movement Isolated in soil, water, and vegetation Disease assoc. with consumption of contaminated food products (unpasteurized milk) Transplacental spread from mother to neonate (vaginal transmission) HIGH RISK: Young, elderly, Pregnant, pts with defective cellular immunity Neonatal Disease ­ Amnionitis: 1. Early onset disease: “granulomatosis infantiseptica” ‐> disseminated ascesses and granulomas in multiple organs 2. Late onset disease: acquired at or shortly after birth. Presents as meningitis or meningoencephalitis w/ septicemia Healthy Adults: Influenza like (with or without gastroenteritis) Pregnant women/cell­mediated immune defects: Primary bacteremia or disseminated disease (hypotension and meningitis) Microscopy ‐> insensitive Culture 2‐3 days or cold enrichment Mycobacteria Tuberculosis Gram (+) Weakly Obligate Aerobes Acid­Fast – cell wall has a lot of lipid in it, which makes it poorly gram staining Facultatively Intracellular (causes granuloma) Mycobacteria Leprae Obligate Intracellular Grows only at cooler temperature (which is why it effects the skin and not the internal organs) Slowest Growing Bacteria (doubling time of 2 weeks) Cord Factor – serpentine growth in culture and inhibits PMN migration. It is the mycolic acid Mycolic Acid – TB is made of primarily fat in its cell wall. The fat happens to be mycolic acid. Peptidoglycan Layer ‐ it is partially gram + and this is because of its peptidoglycan layer beneath its fatty cell wall Tuberculin – protein secreted used to do the PPD test. Sulfatides – glycolipids in cell wall that inhibit phagolysomal fusion, increasing longevity in macrophages Reactive O2 and N2 species survives the oxidative burst None listed in Class nor Kaplan Humans are the only known reservoir. Aerosolized particles are released by an infected patient only in the active form of TB. Therefore, most infections are generally reinfections. Requires a large infectious dose over a prolonged exposure PPD Test: assess exposure to TB by giving the protein Tuberculin in a Subdermal injection. It is a Type IV hypersensitivity High risk: (AIDS)>5mm Moderate Risk (health care worker / inmate / regular exposure) >10mm Low Risk: (general population) >15mm TB – there is no exotoxin, there is no endotoxin, the damage that TB does is the damage the immune system causes in an attempt to get rid of the disease. Macrophages wall it off in a granuloma. Primary TB – recent exposure, currently active, transmittable, growing in macrophage Active TB – Lung Disease, X‐ray Changes, Liquefactive Granulomas (with hemoptysis) Latent TB – Non contagious, calcified granulomas. When immunocompromised it will revert to Primary TB. Reactivation – Latent to Active. These are a type 1 immune response mediated by Th1 cells (compare to leprosy) Sensitive to UV Light Auramine­Rhodamine is a rapid test to see if there are mycobacteria. This stain turns TB bright apple green. BCG vaccine is a live attenuated vaccine given in third world countries that protect against systemic TB, not so much the Pulmonary TB. Treated with a combination of Isoniazid and Rifampin. Caution when treating RA patients with TNF‐α antagonists; TNF‐α keeps the TB contained. Armadillos have Leprae. Humans are the usual reservoir, which requires significantly prolonged exposure. The lapromin test is the analogous test to the tuberculin test (PPD) of tuberculosis. It will be positive only for the tuberculoid leprosy because it shows an active immune response. Tuberculoid Leprosy – strong immune system. This is a Th1 response. It contains the disease by forming granulomas in the nervous tissue. It causes patches of anesthesia as the immune system walls of the leprae in the nerves. Lepromatous Leprosy – weak immune system. This is a Th2 response and is a wild dissemination. There will be nodular skin lesions with multiple organ involvement. This causes the “lion‐like” facial lesions that are associated with the severe form. Dapsone and Rifampin that has to be taken over 2 years to eliminate the disease. Close household contacts will receive prohphylactic Dapsone. Isolation is not required (leper colonies are archaic) Gram Negative Cocci: Neisseria and Moraxella Organism Neisseria Meningitidis Neiserria Gonorrhea High‐Yield image is a gram stain of exudate from someone with gonnorhea with the gram negative diplococci INSIDE the PMNs Moraxella Catarrhalis Previous low‐
yield organism, that has been coming up on the boards Physiology/Structure Gram (­) Cocci Diplococci with flattened sides Oxidase (+) Glu +, Maltose+ Facultative Intrallecular Found in respiratory tract and causes meningitis Gram (­) Cocci Diplococci with flattened sides Oxidase (+) Glu+ Maltose­ Facultative Intracellular Found in the urogenital tract and causes gonorrhea Gram (­) Cocci Diplococcus Virulence Capsule – 5 different serotypes of capsule. B is the most common found in the US. It is NOT covered in the vaccine, but all others are. IgA Protease – helps colonize the respiratory epithelium Endotoxin = LPS Pili for attachment Epidemiology Found in the human nasopharynx. About 5‐10% are carriers of the organism. Usually transmitted through respiratory droplets that colonizes the pharynx and spreads to the menignese. College Dorms, Military Recruits other close quarters Diseases Adult Meningitis Begins with a Stiff Neck, Photophobia Petechial Rash. Once the rash starts, the patient declines rapidly. Fulminant cases develop bruising, DIC, and death. This can happen in hours. Diagnosis Formerly Penicillin (which may still work). Currently use doxycyline or cirpofloxain. Vaccine is available that is a the polysaccharide capsular vaccine covering all types not B. No Capsule Antigenic Variation – changes its antigen to avoid detection Outer Membrane Proteins (OMP) OMP 1 = Por Protein that decreases phagolysosome fusion in PMNs and increases transcytosis OMP 2 = Opa = adhesion molecule IgA Protease ‐ evades mucosal epithelium defenses. Pili ‐ increase adhesion Human genital tract and is transmitted as an STD or to a child in birth. Gonorrhea ‐
Males = urethritis and proctitis. Purulent yellow discharge with painful urination. ‐
Females = variable symptoms including Pelvic Inflammatory Disease, Salpingitis, and Intramenstrual Bleeding. It may go unnoticed, and females are often the carriers ‐
Infants ‐ opthalmia and blindness if untreated Beta‐Lactamases are abundant, so we now use cephalosporins. There is a special agar called Thayer­Martin Agar that is a chocolate agar + antibiotics that grows only gonorrhea Normal flora of the upper respiratory tract Transmited through the respiratory droplets Otitis Media – strep pneumo is the most common cause, but Moraxella can cause ear aches Sinusitis – same thing as Otitis Media Bronchitis – especially in the older population Augementin or third generation cephalosporing Gram Negative Rods – all gram negative bacteria have LPS, the endotoxin, which poses a risk of sepsis, shock, and death Organism Yersinia Pestis Enterobacteriaciae family Physiology/Structure Gram (­) Rod Bipolar Staining, they look like a safety pin or a dumbbell. There is staining at either end, but clear in the middle. Facultative Intracellular – produces granulomas Gram (‐) Rods Catalase (+) Fermenters – at least Glu+ Escherlichia Coli (E.Coli) Same As Enterobacteriaciae family. ETEC Enterotoxigenic E. Coli Same As Enterobacteriaciae family. EHEC EnteroHemorrhagic E. Coli Same As Enterobacteriaciae family. Know the O157:H7 serotype is the most implicated. Non­Sorbitol fermenter (most E.Coli are sorbitol Virulence Coagulase (+) F1 Antigen can inhibit phagocytosis Type III Secretion System – molecular syringe that allows for toxins to be injected into host cell. Epidemiology Cause of the plague, the black death. Common in the desert southwest. Transmitted by the bite of a flea or by human‐
human contact via respiratory droplets Endotoxin – all gram negative bacteria possess LPS or LOS. Antigens: O = Cell Wall K = Kapsular H = Flagella Pili – attach and establish infection in the mucosa of the GI tract or the urinary tract. Capsule ‐ Enterotoxins they are cyclic‐something inducers. One is cAMP, the other is cGMP. Regardless of the mechanism, they both cause watery diarrhea. Heat Labile Toxin– (LT) causes ADP‐Ribosylation of Gαs that stimulates AC Æ cAMP Heat Stabile Toxin– (ST) causes ADP‐Ribosylation of Guanine Cyclase increasing cGMP. Shigga­Like Toxin – a classic AB toxin that causes ADP­Robsylation of the 60s ribosome reducing affinity for EF­1. Called verotoxin. Diseases Pneumonic Plague =septic pulmonary embolus from the bubonic plague, or inhalation. This is highly contagious, highly fatal, and is a target of bioterrorism Cutaneous = Bubonic Plaque = Black Death. This is from the flea bites that generate the axillary bubos and conjunctivitis. Its called the Black death because you get DIC and the extremities, without an adequate blood supply, necrose, turn black, and fall off. Diagnosis Tx Aminoglycosides Control the animals, the vector (the rats). Killing rodents is a bad idea, the fleas will all go to humans! Normal flora of the human Gut. There can be an engodenous displacement from the GI (such as in UTI) or can be exogenous (such as fecal oral) Same as E. Coli Most common cause of UTI. Neonatal meningitis. This is the second most common cause of neonatal meningitides after Strep Agalactiae. K1 serotype implicated. Fluroquinolone Third generation cephalosporin Montezuma’s Revenge. ETEC causes Travler’s Diarrhea. This is a watery diarrhea because it is noninvasive. Usually Self Limiting. Replace fluids either IV or Oral. Same as E.Coli, but can also be from bovine feces or unpasteurized milk. EHEC can be remembered as Hamburger (the Jack‐
in‐the‐Box E. Coli outbreak). Dysentery. EHEC causes Hemorrhagic diarrhea. This is an exception to the rule. Normally bloody diarrhea means invasive organisms. This is non invasive. Therefore, there will be (+) Blood (­) Pus. Hemolytic Uremic Syndrome (HUS). A sequella of EHEC is renal failure. DO NOT GIVE ANTIBIOTICS. Death of EHEC will release its toxin and LPS that increases the risk of HUS. EIEC & EPEC Salmonella Enteriticus fermenter) Low‐yield without detail Gram (‐) Rods Motile (like a salmon) Lac – Facultative Intracellular Salmonella Typhi Gram (‐) Rods Motile (like a salmon) Lac – Facultative Intracellular Shigella Gram (­) Rods Nonmotile No H2S Non‐Lactose Fermenters Facultative Intracellular Klebsiella Pneumoniae Gram (­) rod, part of the enterobacteriacae They are in here to make you aware that it exists. Don’t know them for Tulane exams. Salmonellosis = Gastroenteritis potentially Acid Tolerance Response Does have an animal causes bloody diarrhea (it is invasive), but reservoir. Found on eggs, usually causes a watery diarrhea. Causes Pili poultry, reptiles, diarrhea by an increase in cAMP as a result of including reptile feces. inflammation NOT a result of exotoxin. LPS Osteomyletis – most common cause of This is the undercooked osteomyletis in those with sickle cell. chicken disease Without sickle cell, the most common cause is Staph Aureus. Typhoid Fever – typhoid = typhus‐like. Has no animal reservoir, Acid Tolerance Response Organism is ingested with infection in the Gene. Decreases in pH cause thus vaccines are ileocecal region. This causes constipation. available. the gene to turn on, Travel + Constipation = Typhoid. increasing defense, Humans have it in their GI decreasing virulence (it M cells take up the cells via phagocytosis. It is tract, or survivors of survives in, but does not presented to macrophages where it survives Typhoid Fever contain it infect, the stomach). within the phagolysosome. The macrophage within Increases in pH cause the transports it to lymph nodes and to the gene to turn off, decreasing spleen, where it enters circulation. defense, increasing virulence (it colonizes the It can reenter the GI tract through the Gall intestines). This is also how Bladder, where it can take up permanent it lives within the lysosome. infection and create a carrier state. Vi Antigen (Typhi only). It Systemic infections cause rose­pedal lesions is the Kapsular antigen, but given a special name in which are pinpoint erythmatous lesions on salmonella. Withstands the trunk or abdomen. phagocytosis and complement destruction. Septecemia is possible. Adhesins/Pili allow adhesion to the mucosal epithelium Shigella Soneii is the most Dysentery – aptly named Dysenteriae. Causes Shigga Toxin – Classic AB a bloody diarrhea. It is invasive and kills cells common in US and is the toxin. ADP‐Ribosylates the leading to the blood. The inflammation least virulent. 60s ribosome reducing the response causes the malabsorption and affinity for EF‐1 diarrhea. Shigella Dysenteriae is the worst of the shigellas, Invades M cells by Can lead to Hemolytic Uremic Syndrome, but is uncommon in the phagocytosis, then migrates which is normally associated with EHEC. US into neighboring cells However, since the toxins are so similar, the There are no animal intracellularly. It can also carriers. The human colon possibility for HUS is present. live within the macrophage is the only reservoir. by escaping the Transmission is fecal‐oral, phagolysosome. When the such as at day care macrophage finally lyses, shigella is able to get into epithelial cells via the basal surface Hugely pathogenic, incredibly low infectious dose (1‐10 organisms) Capsule – antiphagocytic Found in colon and upper Number one cause of aspiration pneumonia and antigenic. respiratory tract. in alcoholics. Invasive disease fluroquinolone If it is only local in the GI tract, don’t treat it. If they go systemic, use Beta‐Lactams and Fluorquinolones. There are vaccines available ‐
ViCPS = capsular vaccine, administered parenterally ‐
Ty2a1 = attenuated bacteria ingested many times to develop adequate resistance ‐
Either are given to people traveling to endemic areas. Usually self‐limiting. Antibiotics can be used, but multiple drug resistances make it challenging to eradicate. Fluroquinilone or In culture will have a halo around cells, because of their capsule. Lac+ Endotoxin –LPS from it being Gram (‐) Usually an endogenous transmission Community acquired pneumonia. Common cause of community acquired. Strep Pneumo is the most common cause, but Klebsiella is still right there. Use the gram stain to separate. Causes a thick like jelly, red sputum without a pungent odor (such as in the case of a aspiration pneumonia). Rapidly Spreading Cellulitis from the site of the lick or bite, there will be a cellulitis that will spread within hours. Third generation Cephalosporin Pasturella Multocida think CATS and CAT BITES Small Gram (­) Rods Facultative Intracellular facultative Anaerobe Reservoir is the mouths of cats, transmitted from bites or licks. Don’t confuse this with Cat‐
Scratch fever, which is caused by a scratch, not a lick or a bite like Pasturella Bordetella Pertussis Small gram (­) rod Nonmitile Strictly Aerobic Grow Singly or in pairs Encapsulated Requires a long growth period on a special agar, called the Bordet­Gengou Bordet = Bordetella Vibrio Cholera Curved, Gram (­) Rod with polar flagella Oxidase (+) Grow on Alkaline but not Acidic Motile Pertussis Toxin – classic AB toxin that targets the ciliary cells. It is a cAMP toxin, causing edema and fluid. This causes increase in histamine sensitivity, leukocytosis and an increase in insulin, leading to hypoglycemia. Dermonecrotic Toxin Adenylate Cyclase Toxin – secreted AC that is taken up Tracheal Cytotoxin Filamentous Hemagglutin Endotoxin Pilus – the Tcp Pilus allows for adhesion to mucosal epithelium Flagella – makes it motile Toxin – cholera toxin is a classic AB toxin. It activates Gαs via ADP‐Ribosylation. It causes cAMP increases that leads to tremendous fluid extrusion Colonizes the respiratory epithelium and cab be spread via respiratory droplets (the coughing, sneezing, and hand‐to‐
hand contact) Whooping Cough – comes in 3 phases after a week of incubation. ‐
Catarrhal Stage – the highly infectious stage with nonspecific symptoms such as low grade fever, malaise, rhinitis. Weeks 2‐3 ‐
Paroxysmal Stage – this is the noninfectious, but stereotypical phase. This stage has frequent bouts that come and go (paroxysmal) of severe fits of coughing followed by a strong inspiration against a narrowed glottis causing the “whoop.” They can become cyanotic or vomit. Weeks 3‐6 ‐
Convalescence Stage – the disease dies out, with lessening paroxysmal stage symptoms. Weeks 6‐on Erythromycin is drug of choice to give to household contacts and those in the catarrhal phase. Isolate the catarrhal and early paroxysmal phases Vaccinate with the DPT vaccine. The reservoir for cholera is the human colon. It is transmitted fecal‐oral, but often by contaminated water. It requires a very high infectious dose. El Tor strain causes epidemics The classic strain has not been so bad Cholera – excessive diarrhea up to 20L/day. Causes rice water stools, looking white/clear like water while cooking rice. Treat with fluid and electrolyte replacement, both oral and IV. Prevent cholera by boiling water and vegetables, cooking your food Amoxyclin and Augmentin Because it is so rapid spreading, they give an IM injection of antibiotics. Helicobacter Pylori Gram (­) curved rod with a Single polar flagella (sounds like Cholera) Only organism that can grow and replicate in the stomach Proteus Mirabillis and Vulgaris Mirabillis = 90% of infection Small Gram (‐) Rods that are part of the enterobacteriacae family Swarming Motility from its peritrichous flagella Urease + Nonlactose­Fermenting Legionella Slender, pleomorphic, G‐ve rods Stains poorly w/common reagents – Use Silver Stain Nutritionally fastidious ‐> L­cysteine and enhanced growth with iron salts Non fermentative Urease converts urea and acid into bicarbonate and ammonia, which neutralizes the acid, allowing it to live in the stomach Adhesins allow colonization and prevent dislodgement from gastric mucosa Mucinase degrades the mucin protective barrier Vacuolating Cytotoxin induces vacuoles in human cells. Cytoxin Associated Gene encodes another cytotoxin. These HP are more virulent Extreme Motility Urease Endotoxin LPS from gram (‐) Capable of replication in ALVEOLAR MACROPHAGES (and amoebae in nature) Prevents phagolysosome fusion Humans are the only known reservoir and it is thought that it is transmitable fecal to oral or oral to oral. The mode of transmission has not yet been established, despite its prominence in GI disease. Gastric/Duodenal Ulcer – the urease and mucinase degrades the protective lining of the stomach, allowing acid to reach the mucosal surface. In addition, the cytotoxins cause autolysis of macrophages and neutrophils inducing a strong inflammatory reaction, also contributing to the disease. Can lead to cancer. Either the reactive oxygen species damaging DNA post lysis and inflammation or through viral infection of the epithelium from the compromised barrier, gastric tumors may result. This is a Type 1 Carcinogenic Agent, a highly board relevant point. Pretty much ubiquitous in the environment and within the normal flora of the GI tract. Most cases in humans are endogenous. UTI if there is a UTI via proteus (E Coli most common), there is an increased risk of kidney stones by reducing the pH of the urine. Sporadic, epidemic, nosocomial infections Aerosol Transmission (Air conditioning units, but no person to person) Commonly found in natural bodies of water (rivers and streams) Estimated btw 10k to 20k cases in US annually High risk: compromised pulmonary function, pts with decreased cellular immunity (transplant) 1. Legionnaires’ disease (legionellosis) incubation period of 2‐10 days systemic signs of acute illness appear abrupt Multiorgan disease (GI, CNS, liver, Kidneys) Primary manifestation – pneumonia (severe) 2. Pontiac fever Self limiting, febrile illness Fevers, chills, myalgia, malaise, headache Symptoms develop over 12 hrs, last 2‐5 days Serology can detect antibodies, but will only tell you if there ever was an infection. Golden standard is the biopsy with culture. Use the Urea Breath Test to determine if someone has HP. You feed the patient radioactive urea, and, if there is HP, they will expire radioactive CO2 (converted from the bicarb the HP made) Endoscopy can be made to identify gastric ulcers. Treat the ulcers with Proton Pump Inhibitors treating the symptoms. Treat the bug with Amoxicillin + Clarithromycin Fluroquinilone Treat kidney stones with pain meds (for passing) or sonic disruption to remove stones. Microscopy: insensitive DFA – fluorescence Culture: Buffered charcoal yeast extract (BCYE) and Fe+Cys Antigen tests: sensitive for L. pneumophila serogroup 1 Seroconversion: must be demonstrated ‐> 6 mo. To develop PCR: Sensitivity and specificity approaching culture Chlamydia Gram (­) Rods Obligate Intracellular Bacteria Energy parasites Really small, obligate intracellular = cannot see on a gram stain Reticulate Body vs Elementary Bodies Elementary bodies are the metabolically inactive form that infects cells. Reticulate bodies are the metabolically active form within infected cells. Chlamydia Trachomatis Gram (‐) rod Obligate Intracellular (granuloma formation) Reservoir is the genitalia and the eyes. It is can be transmitted via sexual intercourse, hand‐to‐face, or even via flies. Sexual Transmitted Diseases. Most common bacterial STD in the US. Urethritis, cervicitis, and damage to the fallopian tubes. This causes sterility. Serotypes D‐K Lymphogranuloma Venereum – begins with L, so do the seroptypes. Not common in the US, but in developing countries. It is an STD that causes swollen lymph nodes that eventually results in blockage of lymph drainage and genitle elephantiasis. Trachoma ‐ Serotypes A‐C. Results in conjunctival scarring and blindness. It is the most common cause of preventable blindness. Chlamydia Pneumo Treponema pallidum Gram (­) Spirochete Really had to find on a gram stain. Obligate Pathogen (we cannot culture it). It is NOT an obligate intracellular pathogen. Human genital tract is the reservoir. It is a sexually transmitted disease that can be passed to the fetus. Syphillus – has 3 stages (1) Primary – non­tender chancer. There is no pain, the lesion is there, after a few weeks goes away. If you biopsy the lesion you could see the treponema. Serologic tests will stay negative. (2) Secondary – maculopapulo copper colored rash that is diffuse that includes palms and soles, with patchy alopecia. This rash is capable of transmitting disease. Condylamata looks like HPV with warts growing in the perianal region. Serology comes back positive. (3) Tertiary ‐ syphilitic granunlomas (aortictitus, Tabes Dorsalis, and altered Primary: Newer macrolides or fluoroquinolones ie. Azithromycin, clarithromycin or ciprofloxacin, levoloxacin Decreased environmental exposure to reduce risk of disease Water: treat with hyperchlorination, superheating, copper‐silver ionization Decontaminate air conditioning units. Two types of tests to do to diagnosis: (1) Screening: crossacting antibodies to cardiolipin. nonspecific, cardiolipin, VDRL (caution SLE which may yield false negative) (2) Specific : immunofluorescence FTA­ABS Penicillin is the treatment. Even if allergic, the treatment is penicillin. Doxycyline to treat disease Erythromycin can be given prophylatically. Borrelia Burgdorferi Gram (­) Spirochete It is invasive, and will infect the heart, joint, and CNS. Nymphs (on mice) and Ticks (on deer). We usually here about this disease with deer ticks from Lyme CT. Ixodes is the genus of tick that spreads the organism. Leptospira interrogans Low yield Spirochete Gram (­) Spirochete, with little hooks at the end Unknown pathogenesis Rickettsia Rickettsia Ricketsii Energy parasite. They need your ATP, and are an obligate intracellular parasite with leaky epithelium Very tiny, so you wouldn’t see them on a gram stain, even though they are considered Gram (­) rods Invade the vascular endothelial cells causing vasculitis and permitting them to move through the blood strea, Zoonotic disease with transmission through water contaminated with animal urine. You will see this in patients who jet ski or who work in sewers. Reservoir is ticks. The vector is a tick bite. Requires a long feeding time in order to transmit the bacteria. The bacteria may be passed to progeny. Rickettsia Prowazekii Considered low yield for Boards Rickettsia Typhi Considered low yield for Boards Haemophilus (and related bacteria) Same as Ricketsii Same as Ricketsii Small, pleomorphic, G­ve rods or coccobacili Facultative anaerobes, fermentative Most species require X (heme) and/or V (NAD) factor for growth H. influenzae subdivided serologically (a to f), biochemically (biotypes I to mental states). Lyme Disease – This is the number 1 vector‐borne disease. You get a bulls­eye rash at the bite site. It starts out with flu‐like symptoms with swollen lymph. Once the organism disseminates, then you see nerve effects (such as bell’s palsy). Migratory Arthralgia develops from Type III hypersentivity reactions depositing into the joints. Cardiac Arrythmias may result from the disease as well. Swineherd’s Disease or Mud Fever – gastrointestinal symptoms + flu‐like symptoms that may progress to hepatic or liver failure. Serology diagnoses the problem via ELISA or PCR. Treatment is doxycycline Rocky Mountain Spotted Fever. Rash is critical for the diagnosis. When not present, the disease is usually missed until too late, as this disease is rapidly fatal. Confusion, N/V/D + headache. It looks like meningitis, but then the rash comes on. The rash is a maculopapular that turns petechial that starts on the hands and feet and moves to the trunk. Includes palms and soles Endemic Typhus Start treatment without confirmation from serological indirect antibody test. Weil‐Felix is an old test, that might creep on the boards. H. influenze type b is clinically most virulent (PRP – polyribitol phosphate – in capsule) PRP – ribose, ribitol, phosphate Haemophilus adhere to host cells via pili and non‐pilus structures IgA Protease Noncapsular Haemophilis commonly colonized in humans; encapsulated Haemophilis (H. influenze type b) UNCOMMON members of normal flora Disease caused by H. influenze type b was primary a pediatric problem ‐> eliminated in immunized populations Haemophilis influenzae Meningitis: unimmunized children ‐> fever, severe headache, systemic signs Epiglottitis: unimmunized children ‐> initial pharyngitis, fever, difficulty breathing, progresses to cellulitis and swelling of supraglottic tissues ‐> obstruction of airway Pneumonia: inflammation and consolidation of lungs observed primarily in the ELDERLY with underlying chronic pulmonary disease; typically caused by nontypeable strains Haemophilus ducreyi Microscopy – sensitive test in CSF, synovial fluid, lower respiratory specimens Culture ‐> chocolate agar Antigen tests‐> less useful for H. influenzae type b infections Doxyclcine and protection against the vector. Bacteroides Fragilis VIII), and clinically (biogroup aegypticus) Satellite Phenomena – you can grow Haemophilus next to staph because it is beta‐hemolytic and releases the heme and NAD into the medium on a blood agar. Gram (­) Rod Reduced Endotoxin Capsule H. ducreyi disease is uncommon in the US With the exception of H. ducreyi, which is spread by sexual contact, most Haemophilus infections are cased by pts bacterial flora (endogenous infections) Normal part of the GI flora. Traumatic displacement (surgery) can permit movement into other compartments. Francisella Tularensis (potentially low­
yield accept it is a Bioterror agent) Zoonotic Small Gram (­) Rod Facultative Intracellular pathogens (cause granulomas) Tick bite (the ulcero‐
glandular form) Associated with hunting and skinning Wabbits. This can cause a traumatic implanation or inhalation while you shred its flesh everywhere. If you eat the rabbit without cooking it well, you could ingest it as well Brucella (potentially low­
yield accept it is a Bioterror agent) Zoonotic Small Gram (­) Rod Facultative Intracellular pathogens (cause granulomas) Endotoxin – LPS in gram (‐) Passes readily between animals and humans. Usually contained in domestic livestock (large animal veterinarians) Species depends on the animal it infects. Abrotus = cattle Sewis = pigs Malatensis = goats Chancroid: STD ‐> tender papule with an erythematous base ‐> progresses to painful ulceration and lympathadenopathy. This is a distractor with Syphilis (treponema) because they are both spirochetes, and both cause a chancer. Yoyu “do cry with ducreyi” meaning that it is a painful chancer. following vaccine Sepsis: weak, because the endotoxin is modified. Peritonitis: This isn’t terribly high yield, but man you don’t want this kind of peritonitis. It will cause massive necrosis of the peritoneum and the intrabdominal contents Tuleremia: Ulcer at bite site and regional lymph swelling from tick. Traumatic Implantation from wabbit skinning can cause it as well. If you inhale it or eat it, you will develop tularemia in the GI tract. Live Attenuated Vaccine broad‐spectrum cephalosporins, azithromycin, or fluoroquinolones Many strains are resistant to ampicillin Active immunization with conjugated PRP vaccines prevents most H. influenzae type b infections Rifampin prophylaxis ‐> children at high risk for disease Brucellosis – undulant fever because it goes up and down. They are flu‐like symptoms with profuse sweating. Serum Agglutination test is pretty much all you can do. Rifampin & Doxycycline for 6 weeks (facultative intracellular are tough) We can vaccinate cattle or high risk individuals. Pasturization helps spread. Gram Positive Cocci ‐ Staph = Aureus, Epidermis, ‐ Strep = Pyogenes, Agalactiae, Mutans (Viridans group), Pneumonia, Enterococcus Gram Negative Cocci “Never mind about Moraxella” NM, The N and M that aren’t in the Ram Positive Rods. ‐ Neisseria = Gonorrhea, Meningitidis ‐ Moraxella = Catarrhalis Gram Positive Rods “BCC: LAN, LM”, “Send an email (BCC) over the network (LAN) to Lincoln Martin (LM)” B of BCC ‐ Bacillus = Anthracis, Cereus C of BCC ‐ Corynebacterium = Diphtheriae C of BCC ‐ Clostridium = Tetani, Botulinum, Perfringes, Difficile La of LAN ‐ Lactobacillus = Lactobacillus A of LAN ‐ Actinomyces = Israelii N of LAN ‐ Nocardia = Nocardia Li of Lincoln, also think “listserv” ‐ Listeria = Monocytogenes M of Martin ‐ Mycobacteria = Tuberculosis, Leprae Gram Negative Rods Everything else. Yep, that’s right. Everything. I hate memorizing lists (like all bacteria above), so here some categorizations to help you keep the bugs straight Non‐Enteric Gram Negative Rods Respiratory
Haemophilus Influenzae Legionella Pneumophilia Bordetella Pertussis cAMP Vibrio Cholera ETEC Bacillus Anthracis Toxin Secreting Protein Synthesis Inhibition Corynebacterium Diphtheria EHEC Bordertella Pertussis Pseudomonas Shigella Neurotoxins
Clostridium Tetanii
Clostridium Botulinum Zoontic
Francisella Tularensis
Pasturella Multocida Brucella Spp. Yersinia Pestis Rickettsia Rickettsii Rickettsia Prowazekki Coxiella Bartonella Opportunistic
Pseudomonas Aeruginosa
Klebsiella Pneumoniae Enterobacteriaciae Nonlactose Fermenters “ShYPS” Shigella Non motile, non H2S producing Yersinia Proteus Motile, H2S producing Salmonella Spore Formers “Start off the Gram Positive Rods” Bacillus Clostridium Capsules: “Some Killers Have Pretty Nice Capsules” S – S. Pyogenes K – Klebsiella Pneumoniae H – Haemophilus Influenza P – Pseudomonas Aeruginosa N – Neisseria (Meningiditis only) C – Cryptococcus (fungus) Lactose Fermenters – “CEEK” Citrobacter – Tulane doesn’t discuss it Escherichia – E Coli Enterobacter Klebsiella Urease Positive
Klebsiella Pneumoniae Helicobacter Pylori Proteus Toxins Intracellular Growth
Facultative Listeria Monocytogenes Salmonella Genus Shigella Genus Mycobacteria TB Brucella Genus Bartonella The “ABCs” of Anaerobic bacteria A – Actinomyces (gram +) B – Bacteroides C – Clostridium (gram +) Acid Fast Bacteria Mycobacteria (TB and Leprosy) Nocardia Obligate Mycobacteria Leprae Rickettsia Rickettsii Coxiella Burnetti Erlichia Chlamydia Species