Microbiology Hell – Flashcards
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Unlock answers  Streptococcal Pharyngitis (Caustive Agent) |
 - Streptococcus Pyogenes Gram-positive ? hemolytic |
  Streptococcal Pharyngitis (Symptoms) |
Symptoms:Â Sore, red throat, with pus and tiny hemorrhages, enlargement and tenderness of lymph nodes in the neck; less frequently, abscess formation involving tonsils; occasionally, rheumatic fever and glomerulonephritis as sequels. |
 Streptococcal Pharyngitis (Pathogenesis) |
 –Causes a wide variety of illnesses (due to toxins and exoenzymes)  –Complications of infection can occur during acute illness |
    Streptococcal Pharyngitis (Epidemiology) |
 –Spread readily by respiratory droplets •Especially in range of 2 to 5 feet –Infect only humans under natural conditions –Nasal organism spreads more effectively than pharyngeal carriers –Peak incidence occurs in winter or spring •Highest in grade school children |
Streptococcal Pharyngitis (Prevention) |
 –No vaccine available –Adequate ventilation –Avoid crowds  –Sore throats in presence of fever should be cultured for prompt treatment |
  Streptococcal Pharyngitis (Treatment) |
–Confirmed strep throat treated with 10 days of antibiotics •Penicillin or erythromycin are drugs of choice  –Eliminates organisms in 90% of cases |
Common Colds (Causative Agent) |
 –30% to 50% caused by rhinovirus •Non-enveloped  •Single-stranded RNA genome |
Common Cold (Pathogenesis) |
 –Virus attaches to specific receptors on respiratory epithelial cells and multiplies in cells •Large number of viruses released from infected cells –Injured cells cause inflammation which stimulates profuse nasal secretion, sneezing and tissue swelling –Infection is halted by inflammatory response, interferon release and immune response  •Infection can extend to ears, sinuses and lower respiratory tract before stopping |
   Common Cold (Epidemiology) |
 –Humans are only source for virus –Close contact with infected person or secretions usually necessary for transmission •High concentrations are found in nasal secretions during first 2 or 3 days of it Young children transmit it easily |
 Common Cold (Symptom) |
  Scratchy throat, nasal discharge, malaise, headache, cough |
 Common Cold (Prevention) |
 –No vaccine •Too many different types of rhinovirus  - directed at •Hand washing •Keeping hands away from face  •Avoiding crowds during times when colds are prevalent -Treatment –Antibiotic therapy is ineffectual –Certain antiviral medications show promise •Must be taken at first onset of symptoms –Treatment with over-the-counter medications may prolong duration due to inhibition of inflammation |
Pinkeye, Earache and (Causative Agent) |
 –Haemophilus influenza •Gram-negative bacillus –Streptococcus pneumoniae •Gram-positive diplococci –Otitis media and sinusitis •Mycoplasma pneumoniae •Streptococcus pyogenes •Staphylococcus aureus  –One-third of cases of otitis media have viral etiology |
   Pinkeye (Pathogenesis) |
  –Most likely from airborne respiratory droplets  –Resist destruction by lysozyme |
  Earache (Pathogenesis) |
 •Often developing at the time of conjunctivitis diagnosis •Begins with infection of nasal chamber and nasopharynx  |
  Sinus Infection (Pathogenesis) (( |
  •Begins with infection of nasopharynx and spreads upwards  •Pathogenesis mechanism much like that of otitis media |
Pinkeye, Earache and (Epidemiology) |
 –Carrier rates of H. influenza  and   S. pneumoniae can reach 80% –Epidemics of pinkeye common among school children •Generally in crowded environments –Otitis media very common in early childhood •Older children develop immunity to H. influenza –Less common cause of earache after age five –Sinusitis occurs in adults and older children  •Generally due to more developed sinuses |
  Pinkeye (Prevention and Treatment) |
 •Prevention is directed towards –Removal of infected individuals from school or day care –Hand washing –Avoid rubbing or touching eyes –Avoid sharing towels Treatment is achieved through eyedrops or ointments containing antibacterial medications |
  Earache (Prevention and Treatment) |
 •Prevention is directed towards –Administration of influenza vaccine to infants in day care facilities during “flu” season  •Treatment includes –Antibiotic therapy  »Amoxicillin |
  Sinus Infection (Treatment and Prevention) |
 •There are no proven preventative measures •Treatment is directed at support care –Decongestants and antihistamines are generally discouraged  »Ineffective and can be harmful |
  Pneumonia (Causative agents) |
 –Streptococcus pnuemoniae •Gram-positive •Capsule responsible for virulence •80 different types of   S. pneumoniae –Klebsiellapneumoniae •Gram-negative •Bacillus •Encapsulated –Mycoplasma pneumoniae •Deformed bacterial lacking cell wall  •Aerobic |
  Pneumonia (Epidemiology) |
 –30% of healthy individuals carry encapsulated strain in their throat  •Bacterial rarely reach lung due to mucociliary escalator |
  Whooping Cough (Causative Agent) |
 –Bordetella pertussis •Encapsulated •Strictly aerobic •Gram-negative •Bacillus -> endo spores  •Does not survive long periods outside the host |
  Whooping Cough (Pathogenesis) |
 –B. pertussis produces numerous toxic products (A-B toxin) -B portion attaches to cell surface -A portion enters cell »Causes increased mucus formation  »Decreases phagocytic killing |
  Whooping Cough (Epidemiology) |
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Whooping Cough (Prevention) |
–Directed at vaccination of infants •Prevents disease in 70% of individuals •Pertussis vaccine combined with diphtheria and tetanus toxoids (DPT)  –Injections given at 6 weeks, 4, 6 and 18 months |
  Whooping Cough (Treatment) |
 –Erythromycin is effective at reducing symptoms if given early  –Antibiotic usually eliminates bacteria from respiratory secretions |
  Whooping Cough (Symptoms) |
 Violent coughing, vomiting and possible convulsions |
  Tuberculosis (Causative Agent) |
 –Mycobacterium tuberculosis •Gram-positive, bacillus •Acid fast due •Slow growing –Generation time 12 hours or more  •Resists most prevention methods of control |
  Tuberculosis (Symptoms) |
 –Chronic illness –Symptoms include •Slight fever with night sweats •Progressive weight loss •Chronic productive cough  –Sputum often blood streaked |
  Tuberculosis (Pathogenesis) |
 –Usually contracted by inhalation of airborne organisms –Bacteria are taken up by pulmonary macrophages in the lungs then sent to lymph nodes –Resists destruction within phagocyte  –About 2 weeks post infection intense immune reaction occurs |
  Tuberculosis (Epidemiology) |
 –Estimated 10 million Americans infected •Rate highest among non-white, elderly poor people –Small infecting dose •ID 10 (inhaled) –Factors important in transmission  •Frequency of coughing, adequacy of ventilation, degree of crowding |
Tuberculosis (Prevention) |
 –Vaccination widely used in many parts of the world  •Vaccine not given in US because it eliminates use of a test as diagnostic tool |
  Tuberculosis (Treatment) |
 –Antibiotic treatment is given in active cases •Two or more medications are given together to reduce potential antimicrobial resistance •Antimicrobials include –Rifampin and Isoniazid (INH) •Therapy is prolonged  –Lasting at least 6 months |
  Influenza (Causative Agent) |
 –Influenza A virus •Single-stranded RNA genome –Genome divided into 8 segments •Spiked envelope –H spike – hemagglutinin »Aids in attachment »N spikes – neuraminidase  »Aids in viral spread |
  Influenza (Pathogenesis) |
 –Acquired through inhalation of infected respiratory secretions –Infected cells die and slough off •Destroy mucociliary escalator –Host immunity quickly controls viral spread  –Small number of people die from it |
  Influenza (Epidemiology) |
–Outbreaks occur in United States every year •Associated with 10,000 to 40,000 deaths –Pandemics occur periodically •Most “famous” pandemic of 1918 –Spanned the globe in 9 months  •Pandemics have higher than normal morbidity |
  Influenza (Prevention and Treatment) |
 –Vaccine can be 80% to 90% effective –New vaccine required every year •Due to antigenic drift •Antiviral medications are 70% to 90% effective •Must be taken early  •Not a substitute for vaccine |
  Rocky Mountain Spotted Fever (Symptoms) |
 –Distinguished by initial rash of faint pink spots •Appears first on palms, wrists, ankles and soles of feet  –Rash becomes raised and hemorrhagic, eventually spreads to other parts of the body |
  Rocky Mountain Spotted Fever (Causative Agent) |
 –Rickettsia rickettsii –Obligate, intracellular bacterium •Requires host organism for survival –Gram-negative, non-motile, coccobacillus -> endospores  •Bacteria are very small and often difficult to see in gram stain |
  Rocky Mountain Spotted Fever (Pathogenesis) |
 –Disease acquired from bite of a tick infected with R. rickettsii –Bacteria are released into blood and taken up by cells lining vessels –Bacteria enter cells through endocytosis •After endocytosis, cell leaves protective phagosome –Bacterial endotoxin released in bloodstream can cause disseminated intravascular coagulation  •This is recognized by shock and generalized bleeding |
  Rocky Mountain Spotted Fever (Epidemiology) |
  - A zoonosis transmitted by bite of infected tick, usually Dermacentor sp. |
   Rocky Mountain Spotted Fever (Prevention) |
 Avoidance of tick-infested areas, use of tick repellent, removal of ticks within 4 hrs of exposure |
   Rocky Mountain Spotted Fever (Treatment) |
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  Lyme Disease (Symptoms) |
 –First Stage •Characterized by skin rash that enlarges •Other influenza-like symptoms can occur –Later Stages  •Heart and nervous system impairment can occur |
  Lyme Disease (Causative Agent) |
–Bacterium called Borreliaburgdorferi –Large microaerophilic spirochete Borrelia genome is linear and has numerous copies |
  Lyme Disease (Epidemiology) |
 Spread by the bite of ticks, lxodes sp., usually found iin association with animals such as white-footed mice and white-tailed deer living in wooded areas |
  Lyme Disease (Pathogenesis) |
 Spirochetes injected into the skin by an infected tick multiply and spread radially; the spirochetes enter the bloodstream and are carred throughout the body; the immune reaction to bacterial antigen causes tissue damage. |
  Lyme Disease (Prevention) |
  Protective clothing; tick repellents. |
  Lyme Disease (Treatment) |
 Doxycycline and others; prolonged antibiotic therapy in chronic cases |
 Cheeeeeekin Pox (Causitive Agent) |
  Varicella-zoster virus; enveloped double-stranded DNA virus of the herpesvirus family |
  Cheeeeeekin Pox (Symptoms) |
 –Skin rash appears on back of head, face and mouth •Rash progresses from red spots called macules to small bumps called papuales to small blisters called vesicles to pus filled blisters called pustules •Lesions itch and appear at different times  •Healing begins after pustules break and crust over |
  Cheeeeeekin Pox (Epidemiology) |
 –Annual incidence once estimated in the several millions but declined due to vaccine –Disease transmitted by respiratory secretions and skin lesions –Incidences increase in winter and spring –Viral incubation period approximately 2 weeks  •Infective 1 to 2 days before rash until blisters crust over |
  Cheeeeeekin Pox (Pathogenesis) |
 Upper respiratory viurs multiplication followed by dissemination via bloodstream to the skin; cytopathic effect of virus includes the formation of giant cells |
  Measles (Symptoms) |
 –Begins with fever, runny nose, cough, red weepy eyes –Fine rash appears within a few days –Symptoms generally disappear within 1 week –Many cases complicated by secondary infections  •Pneumonia and earaches are most common secondary conditions |
  Measles (Causative Agent) |
  Rubeola virus, a single-stranded RNA virus of the paramyxovirus family |
  Measles (Prevention and Treatment) |
  Attenuated virus vaccine after age 12 months; second dose upon entering elementary school or at adolescence. No antiviral treatement available at present. |
  Measles (Pathogenesis) |
 –Infection via respiratory route –Virus replicates in epithelium of upper respiratory tract –Spreads to lymph nodes then to all parts of the body  –Infected mucous membranes important diagnostic sign |
  Measles (Epidemiology) |
 –Humans are only natural host –Outbreaks still occur and are due to non- immune populations –Virus spread by respiratory droplets •Before routine immunization, over 99% of population infected •Vaccine resulted in decline of annual cases  – no longer endemic in United States |
  German Measles (Pathogenesis) |
 –Enters body via respiratory route –Virus multiplies in nasopharynx, then enters bloodstream –Blood transports virus to body tissues  –Immunity develops against viral antigens |
  German Measles (Epidemiology) |
 –Humans are only natural host –Disease is highly contagious •Less so than measles (rubeola) –40% of infected people fail to develop symptoms •These individuals can spread virus  –Infectious 7 days before appearance of rash to 7 days after |
  German Measles (Causative Agent) |
  Rubella virus, an RNA virus of the togavirus family |
  German Measles (Symptoms) |
  Mild fever and cold symptoms, rash beginning on forehead and face, enlarged lymph nodes behind the ears |
   German Measles (Prevention and Treatment) |
  Attenuated rubella virus vaccine administered to children at 12-16 months, repeated at 4-6 yrs of age. No specific antiviral treatment. |
  Tetanus (Causative Agent) |
 –Clostridium tetini •Anaerobic •Gram-negative •Bacillus -> endospores •Spore former •Swarming growth on laboratory media |
  Tetanus (Pathogenesis) |
 –Colonization is generally contained to wound –Bacteria produce toxin –Toxin composed of two chains •Heavy chain binds receptors on motor neuron •Lighter chain taken up through endocytosis –Toxin blocks inhibition of motor neurons, causing paralysis  •Muscle contraction is uncontrolled |
  Tetanus (Symptoms) |
 –Divided into early and late symptoms –Early symptoms •Restlessness •Irritability •Difficulty swallowing •Contraction of jaw muscles •Convulsions Particularly in children –Later symptoms •Increased muscle involvement •Pain •Difficulty breathing  •Death |
  Tetanus (Epidemiology) |
 –C. tetani found in dirt and dust and GI tract of humans and animals –Nearly half of infections result from puncture wounds including •Body piercing, tattooing, animal bites, injected drug abuse –30 to 60 cases in United States annually with 25% mortality rate  –Immunization has decreased incidences in economically advanced countries  |
  Tetanus (Prevention) |
 –Immunization best preventative •Vaccine is inactivated tetanospasmin  –Given in combination with diphtheria and pertusis vaccine – DPT |
  Tetanus (Treatment) |
 –Thoroughly clean wound •Remove all dead tissue –Antimicrobial treatment given to kill multiplying bacteria Metronidazole  Antimicrobials do not kill  endospores Antitoxin - antibody against tetanospasmin  •Neutralizes toxin not attached to nerve cells |
  Gas Gangrene (Symptoms) |
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  Gas Gangrene (Causative Agent) |
  Usually Clostridium perfringens; other clostridia less frequently |
  Gas Gangrene (Pathogenesis) |
 Organism grows in dead and poorly oxygenated tissue and releases a-toxin; toxin kills leukocytes and normal tissue cells by degrading the lecithin component of their cell membranes; invlovement of muscle causes shock by unknown mechanism. |
   Gas Gangrene (Epidemiology) |
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   Gas Gangrene |
Prevention and Treatment Prompt cleaning and debridement of wounds is preventive; no vaccine available. Treatment: surgical removal of dirt and dead tissues of primary importance; hyperbaric oxygen of possible value; antibiotics to kill vegetative C. perfringens of marginal value. |
| Tomato juice agar |
| Selective |
| Blood agar |
| Differential |
| Snyder's agar |
| differential |
| haemophilus influenza |
| Gram negative, bacillus (I have no mnemonic for this one) |
| Streptococcus pneumoniae |
| Gram Positive, diplococci |
| Klebsiellapneumoniae |
| Gram negative bacillus, capsule MNEMONIC: double ll's |
| Mycoplasma pneumoniae |
| Aerobic, lacks cell wall |
| Bordetella pertussis |
| Gram negative, bacillus, capsule MNEMONIC: double ll's |
| Mycobacterium tuberculosis |
| Gram positive bacillus MNEMONIC: there are t's in it, resembling a + sign; "tube" reminds me of a rod-shaped bacillus |
| Pseudomonas aeruginosa |
| Gram negative, bacillus MNEMONIC: no "t" in name, really nasty,thriving on oxygen ruining ppls lives |
| Clostridium tetani |
| Gram negative, anaerobie MNEMONIC: bacteria is shaped like a tennis racket, and a minus sign |
