PID Exam 2

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PID Exam 2
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Infectious Diseases Carver College Medicine Medical School
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Exam 2
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  1. Campylobacter jejuni
    • Description: Slender, spiral-shaped; motile polar flagella; gram negative
    • Oxygen: Microaerophilic
    • Thermophilic, growing at hotter temperatures
    • Oxidase: Positive
    • Clinical: Most common form of acute infectious diarrhea in developed countries; killed by phagocytes and may last 1 to 2 weeks; malaise, fever, and weight loss accompany bloody, loose bowel movements; appears very similar to salmonellosis clinically
    • Diagnosis: Isolate from stool
    • Transmission: Undercooked poultry, water or milk with fecal contamination; stays in GI tracts of birds and non-human mammals; has a low infectious dose, but needs to be ingested with food to protect from stomach acid
    • Guillain-Barre Syndrome: Self-limited, autoimmune disease; neurologic symptoms 1-3 weeks after onset of diarrhea; possibly due to antibody cross-reactivity between O antigens on the bacterial surface and peripheral nerve glycolipids or myelin proteins
    • Virulence Factors: Has the normal things of gram-negatives, but not sure what is the main cause of symptomatic disease (LPS, adhesins, cytotoxic enzymes, enterotoxins); uses flagella to move, invade, and proliferate in intestinal epithelium; adheres to endothelial/epithelial cels and enters in endocytic vacuoles
    • Treatment and prevention: Replace fluids and electrolytes; antibiotics if immunocompromised; thoroughly cooking food
  2. Campylobacter coli
    • Similar to C. jejuni, causing gasteroenteritis
    • Pigs and other livestock are main hosts
  3. Campylobacter upsaliensis
    • Disease similar to C. jejuni, gausing gastroenteritis
    • Dogs and cats may be main hosts
  4. Campylobacter fetus
    • Completely different pattern of disease than C. jejuni
    • May cause miscarriage in pregnant women
    • GI tract of cattle is most likely reservoir
    • Virulence factors: S protein, which acts like a capsule and prevents complement mediated killing
  5. Helicobacter pylori
    • Description: Gram-negative spirals or curved rods; strong swimmer due to 4-7 polar flagella; d
    • Oxygen: Microaerophilic, but must use oxidative metabolism
    • Oxidase: Positive
    • Also has urease, which breaks down urea to make ammonia, allowing it to make a neutral pH around itself in the stomach mucosa
    • Catalase: Positive
    • Clinical: Only bacterium that can colonize stomach; most infections are asymptomatic and this is the most common chronic bacterial infection in humans; causes almost all of chronic inflammation of the stomach antrum, and most of gastric ulcers and duodenal ulcers; is a risk factor for gastric adenocarcinoma and gastric MALT (mucosa-associated lymphoid tissue) B-cell lymphoma; does offer protection from GERD and adenocarcinomas of lower esophagus; this occurs by bacterial release of toxins and exposure of LPS that lead to excess cytokines, causing lymphocytes to harm bacteria and host
    • Diagnosis: CLO test or rapid urease test following gastric biopsy; antigens can be found in stool; antibodies in blood for current or past infections; urea breath test, which tells bacterium is present if labelled CO2 is exhaled
    • Transmission: Fecal-oral route; human stomach is sole reservoir
    • Virulence Factors: Mucinase (degrades gastric mucous and causes localized tissue damage); cytotoxin associated gene (cag) A induces inflammation; urease makes a neutral zone around the bacterium; flagella allow for penetration of mucin layer, which is where they remain for illness;
    • Treatment and Prevention:  Triple or quadruple therapy; no vaccine currently available
  6. Vibrio
    • Description: Short, curved, gram-negative rod with a polar flagellum (contrasted with enterobacteriaceae which are rods with flagella all over)
    • Oxygen:
    • Oxidase: Positive (whereas enterobactericeae are negative)
    • Clinical:
    • Diagnosis: Grows on thiosulfate citrate bile sucrose (TCBS) to distinguish the different types of vibrio; V. cholerae ferment sucrose and appear yellow, whereas V. parahaemolyticus and V. vulnificus do not and look green; on blood agar, vibrios are surrounded by green which is later cleared due to hemodigestion
    • Transmission: Infected water
    • Treatment and Prevention: Clean drinking water; fluids and electrolytes greatly decrease mortality; antibiotics that reduce toxin production are used
  7. Vibrio cholerae
    • Cholera Disease
    • Abrupt onset of watery diarrhea and vomiting; excessive fluid loss leads to colorless, mucous-y stool (rice water stool); can lead to metabolic acidosis, hypokalemia, hypovolemic shock, and renal failure
    • No fever
    • No WBCs in stool
    • Mortality rate is 60% in untreated patients
    • Virulence
    • Toxin co-regulated pilus (TCP) helps bacterium adhere tightly to the mucosal cell layer and prevent being washed out by the fluid production
    • Cholera toxin is an A-B type endotoxin
    • Halotolerant: Can grow in absent of salt
    • Associated with small copepods/shellfish
    • A phage called CTXo inserts the enterotoxin genes into the V. cholerae chromosome when it lysogenizes the bacterium
    • Pandemics
    • Serogroups are based on O antigen, and only O1 and O139 produce the cholera toxin; the O1 subgroup is broken down into serotypes and biotypes
    • Classical Biotype: O1 serogroup, responsible for pandemics 5 and 6 (out of 8 total); "extinct" today
    • El Tor Biotype: O1 serogroup, responsible for pandemic 7 in Indonesia
    • O139: Currenty causing epidemic/endemic disease ("pandemic 8")
    • No protective immunity is conferred from O1 to O139
  8. Cholera toxin
    • Is an A-B type toxin
    • B portion embeds in membrane, forming a pore
    • A is the active subunit, which enters the cytplasm and interacts with and ADP-ribosylates G proteins
    • G proteins then activate adenyl cyclase, resulting in high cAMP, which promotes secretion of flluid and electrolyes in intestinal epithelium, leading to diarrhea
    • This is NOT necessary for production of gastroenteritis/diarrhea, because other toxins also do this
    • Important for the epidemic disease
  9. Vibrio parahaemolyticus and V. vulnificus
    • Halophilic, meaning they require salt for growth
    • Parahaemolyticus: Causes gastroenteritis, wound infection, and bacteremia
    • Vulnificus: More invasive, causing severe diarrhea, septicemia, wound infection, and life-threatening cellulitis; people with renal insufficiency, liver disease, and alcoholism are at risk
  10. Aeromonas hydrophila
    • Description: Gram-negative rods, with polar flagella
    • Oxidase: Positive
    • Belongs to same family as Vibrio
    • Found in fresh and brackish water
    • Causes gastroenteritis: Type 1 has rice-water diarrhea, fever, chills, abdominal pain, nausea, vomiting, and diarrhea; Type 2 has loose stools filled with blood and mucous
    • Halo-intolerant: This is how we can distinguish A. hydrophila from Vibrio and Enterobacteriaceae, which are both able to grow on media containing 6% NaCl
  11. Enterobacteriaceae
    • Description: Include 40 different genera! Gram-negative bacilli
    • Can be opportunistic or overt human pathogens
    • Oxygen: Facultatively anaerobic
    • Oxidase: Negative
    • Catalase: Positive
    • Can ferment glucose, and can grow in the presence of bile that is added to MacConkey and other selective media
    • Can or cannot ferment lactose, breaking them up into two main groups
    • Clinical: Cause gastroenteritis or infections outside the gut, based upon where the bacteria are typically found; if normally found inside the gut, these endogenous bacteria are unlikely to cause gut symptoms and instead cause UTIs, peritonitis, pneumonia, or bacteremia (this is the case for most of the enterobacters)
    • Diagnosis: O antigens (for LPS), H antigens (for flagella), F antigens (for fimbriae/pili), or K/Vi antigens (for capsule) identify organisms
    • Transmission: Found just about everywhere; human carriage in the intestinal tract makes them a common cause of opportunistic infections; transmission happens by fecal-oral route, consumption of contaminated food or water, or direct contact
    • Virulence Factors: LPS, capsular polysaccharide (antiphagocytic), pili for attachment; type III secretion systems; exotoxins; effector proteins; siderophores
    • Treatment and Prevention:
  12. Notable enterics that are lactose positive, aka coliforms
    • Escherichia coli
    • Citrobacter freundii
    • Klebsiella pneumoniae
    • Enterobacter cloacae
    • Serratia marcescens
  13. Notable enterics that are lactose negative
    • Salmonella
    • Shigella species
    • Proteus
    • Providencia stuartii
    • Morganella morganii
  14. Salmonella
    • Description: Enterobacteriaceae; motile, with flagella all over
    • Salmonella enterica; Salmonella bongori is distinct from these, but has never been isolated from disease
    • Oxygen:
    • Oxidase: Negative
    • Catalase: Positive
    • Clinical: Self-limiting gastroenteritis, septicemia, enteric fever syndrome (typhoid fever), or asymptomatic carriage; Salmonella invades the immune system through M cells, which are specialized APCs of the mucosal immune system; invasion of the intestinal epithelium causes necrosis and severe non-bloody diarrhea, vomiting, nausea, fever, cramps, headache, and abdominal pain; can become septic in children, elderly, or immunocompromised
    • Diagnosis: Does not ferment lactose, so appears as pale colonies on MacConkey; appears as blue colonies with black centers on Hektoen-Enteric agar (selective and differential for Salmonella vs Shigella); can grow in presence of bile salts and can produce H2S
    • Transmission: Isolated from reptiles, birds, and non-human mammals; usually enters host during ingestion of contaminated food; survives passage through the stomach; invades intestinal epithelium and reproduces in endocytic vesicles
    • Virulence Factors:
    • Over 2500 serotypes--almost all are S. enterica
    • Treatment and prevention: Fluid and electrolytes; antibiotics for only typhoid fever or specific populations at risk of septicemia from gastroenteritis (otherwise, antibiotics can make people shed Salmonella longer); sanitation and cooking practices help prevent
  15. Enteric fever syndrome
    • Caused by Salmonella enterica strains called S. typhi and S. paratyphi, which are able to survive and grow within macrophages
    • Typhoid fever
    • 21.5 million cases worldwide per year, but only 400 cases in U.S.
    • Clinical: Systemic infection of the lymphatic system following invasion of the intestinal epithelium; NO diarrhea; the symptoms of high fever, headache, malaise, anorexia, and myalgias occur 10-14 days after infection due to severe bacterial growth in blood
    • Asymptomatic Carriage: 3% are long-term carriers who can shed Salmonella from intestines after having or never having symptoms
    • Low infectious dose (10^2-10^5)
    • Fatality rate is 5% treated
    • Virulence Factors: LPS (endotoxin and protects against complement), pili as adherence molecules, pathogenicity island 1 genes (invasion of non-phagocytic cells), pathogenicity island 2 (intracellular survival)
  16. Shigella
    • - Description: Non-motile, non-encapsulated gram-negative rod; serotyping of O antigen breaks genus up into four groups; evolutionarily, the species of Shigella is basically E. coli that has gained the virulence profile through pINV, the invasion plasmid
    • - Does not ferment lactose
    • - Oxygen:
    • - Oxidase: Negative
    • - Catalase:
    • Clinical
    • - Shigellosis; two stages (below); or hemolytic uremic syndrome (HUS)
    • - 1: Short-lasting watery diarrhea and fever following non-invasive colonization and multiplication in the small intestine
    • - 2: Adherence to and tissue invasion of large intestine with typical symptoms of dysentery; frequent stools (>20) with pus and blood (right red, contains fecal leukocytes); daily loss of 200-300mL serum; abdominal cramps; tenesmus (feeling of need to pass stool when rectum is empty), malaise, fatigue, anorexia, nausea and vomiting; usually resolves in 1 week
    • - Diagnosis: Greenish colonies on Hektoen-Enteric agar (whereas salmonella makes bluish-black); lab isolation is needed to distinguish from salmonella or other diarrheal disease-causing bacterium
    • - Transmission: Found only in GI tract of humans, and is transmitted via direct human-to-human contact and the fecal-oral route; really low infective dose (100)
    • - Virulence Factors: Acid tolerance mechanism to survive the stomach; enterotoxin 2 (ShET2, encoded by pINV) plays a role in the initial watery diarrhea phase; type III secretion system which secretes IpaABCD proteins that cause membrane ruffling and engulfment of Shigella; hemolysin allows release of bacteria into cytosol; IpaB induces apoptosis in macrophages and dendritic cells, leading to cytokine release and subsequent damage from inflammation; actin rearrangement encoded by pINV allows for propulsion into neighboring epithelial cells; LPS
    • - Treatment and Prevention: Rehydration therapy; antibiotics; good waste-water treatment, good handwashing, and healthy cooks are prevention measures; vaccines are under development
  17. Shigella dysenteriae
    • Group A shigella
    • Only type that produces shiga toxin, which has neurotoxic, cytotoxic, and enterotoxic effects, allowing very severe disease with a super-fast progression to dysentery
    • Non-mannitol fermenter, whereas the others are
  18. Shigella flexneri
    • Group B shigella
    • Most common worldwide
    • Mannitol fermenter
  19. Shigella boydii
    • Group C shigella
    • Limited to India
    • Mannitol fermenter
  20. Shigella sonnei
    • Group D shigella
    • Most common in U.S.
    • Mannitol fermenter
  21. Escherichia coli
    • Description: Motile (unlike Klebsiella) and produces indole (unlike Enterobacter and Klebsiella)
    • Over 160 knkown O antigen serogroups; are broken down into commensal strains of human gut, pathogenic strains that can cause diseases in the GI tract if enough bacteria are ingested, and pathogenic strains causing extraintestinal infections but no intestinal virulence
    • Oxygen:
    • Oxidase: Negative
    • Catalase:
    • Clinical: Most common causes of diarrhea, gram-negative shock, and urinary tract infections
    • Diagnosis: Lactose fermenter, so appears magenta pink on MacConkey, and orange-salmon on Hektoen-Enteric
    • Transmission:
    • Virulence Factors:
    • Treatment and Prevention:
  22. Escherichia coli pathotypes that are exogenous in nature and have a focus in the gut
    • EIEC
    • Entero-invasive E. coli; non-motile, lactose non-fermenting (unlike all the rest of E. coli)
    • Infections appear identical to Shigella with bloody diarrhea and invation of the large intestine due to invasin genes
    • Has a much higher infectious dose than Shigella (10^6)
    • This type is also exception to rule because it can invade intracellularly
    • ETEC
    • Entero-toxigenic E. coli, aka "Traveler's diarrhea"
    • Prevalent in developing countries and causes sporadic cases of gastroenteritis in the U.S.
    • Abrupt onset of mid to profuse watery diarrhea 1-2 days after ingestion of bacteria and persists for 3-5 days; dehydration, electrolyte imbalance, and hypoglycemia can occur; systemic symptoms such as nausea and vomiting are unlikely
    • Pathophysiology: Adheres to enterocytes, releases ST &/or LT; levels of cAMP and cGMP rise in cells by LT and ST, respectively; hypersecretion of electrolytes occurs; fluid follows
    • Special Virulence Factors: LT (heat-labile enterotoxin) and/or ST (heat stabile enterotoxin) are produced only by ETEC; they both cause fluid secretion; CFAs/CFs are adherence factors
    • Food, water, and ice are vehicles for transmission, but person-to-person transmission does not occur
    • Variable infectious dose (10^2 plus)
    • Bismuth prevents disease by coating stomach/intestine
    • EPEC
    • Entero-pathogenic E. coli
    • Causes infant diarrhea and death in the developing world (rarely seen in older children or adults); non-invasive and non-toxigenic; spread by person-person contact
    • Pathophysiology: Attachment to small intestine via Bfp; normal vili disappear as LEE genes are expressed; microvilli are lost, and an inflammatory response as well as changes in enterocyte permeability/secretion contribute to diarrhea
    • Virulence Factors: Bundle-forming pili (Bfp), LEE pathogenicity island that causes production of intimin (in bacterial membrane on actin "pedestal") and Tir (receptor for intimin that sticks to epithelial cells)
    • EAEC
    • Entero-aggressive E. coli
    • A cause of infant diarrhea (more than 14 days) and growth retardation in developing world
    • AAF1 causes adherence for microcolony formation; EAST, a heat-stable toxin, and PET induce fluid secretion
    • EHEC
    • Entero-hemorrhagic E. coli
    • Dos not ferment sorbitol, and appears colorless on MacConkey sorbital agar, allowing for it to be separated from the other E. coli strains
    • Clinical: Causes bloody dirrhea, non-bloody diarrhea, or hemolytic uremic syndrome (HUS); fever is generally absent, and vomiting occurs in half of the cases; young children are most likely to suffer HUS; DO NOT treat with antibiotics because increases risk of HUS in children
    • This is the most common E. coli diarrheal disease in the developed world, and is spread from the intestinal tract of cattle, sheep, etc by hamburger or produce; some person-to-person transmission
    • Low infectious dose (<100)
    • Virulence Factors: LEE pathogenicity island that became infected with a shiga toxin-encoding bacteriophage; O157:H7
  23. Escherichia coli pathotypes that are endogenous in nature: Extraintestinal pathogenic E. coli (ExPEC)
    • UPEC
    • Uropathogenic E. coli
    • The most common cause of urinary tract infections; uncomplicated cystitis (bladder infection without fever); acute pyelonephritis (kidney infection with fever and chills, nausea, vomiting, and diarrhea)
    • Virulence Factors: Many different combinations, but usually include fimbriae, toxins, siderophores, capsules/serum resistance; usually have pathogenicity islands that set them apart from commensal E. coli strains
    • MNEC
    • Newborn meningitis-associated E. coli
    • The most common cause of gram-negative meningitis in neonates; high fatality rate (40%) and serious sequelae in half of survivors
    • Most subgroups in this class have the K1 capsule type
  24. Escherichia coli Gram-negative shock
    • Need to have a hemolytic toxin (such as RTX)
    • Most cases are associated with an underlying immune-compromising condition, hepatitis, lead poisoning, mushroom poisoning, or cancer drugs
    • Managed with antibiotics and supportive care for hypotension/shock
  25. Klebsiella
    • Description: Enterobacteriaceae; gram-negative rods; prominent capsule, mucoid colonies; non-motile
    • Lactose positive
    • Oxygen:
    • Oxidase:
    • Catalase:
    • Clinical: Nosocomial infections, such as pneumonia, wound infections, urinary tract infections (second most common cause behind E. coli), contamination of IV fluids, and bacteremia/meningitis
    • Diagnosis:
    • Transmission:
    • Virulence Factors:
    • Treatment and Prevention: Resistant to many drugs; go off of local susceptibility patterns to choose drug; do a short course of combination therapy and switch to the specific mono-therapy once the susceptibility is known
  26. Klebsiella pneumoniae
    • Major cause of community- or hospital-acquired pneumonia; mainly affects people with underlying diseases
    • Different from other pneumonias because it causes destructive changes in the lungs
    • Symptoms: High fever, chills, flu-like symptoms, cough productive of mucous which is often thick and blood tinged ("currant jelly"), and necrotic destruction of alveolar spaces
    • High mortality due to the underlying disease persent (>50% even with antibiotics!)
  27. Proteus mirabilis
    • Description: Enterobacteriaceae; gram-negative rods; swarming motility; have urease; H2S positive
    • Lactose negative
    • Is part of normal flora in gut, but pathogenic infections are most often seen in nursing homes and hospitals
    • Oxygen:
    • Oxidase:
    • Catalase:
    • Clinical: Mainly UTIs with formation of urinary stones (from alkaline precipitation of magnesium and calcium), but also causes wound infections, septicemia, and pneumonias (mostly in hospitalized patients)
    • Diagnosis:
    • Transmission: Infected medical equipment including catheters, nebulizers, and examination gloves
    • Virulence Factors: Fimbriae facilitate adherence to uroepithelial cells; urease hydrolizes urea to ammonia to make urine alkaline
    • Treatment and Prevention: Resistant to many drugs; susceptibility tests need to be performed for antibiotic choice
  28. Pseudomonas aeruginosa
    • Description: Gram-negative rods; motile; mucoid exopolysaccharide capsule (slime layer)
    • Oxygen: Aerobes, meaning they can rapidly respire using just about any carbon source
    • Oxidase: Positive
    • Catalase:
    • Clinical: Blue-green pus; significant opportunistic pathogen in burn/immunosuppressive patients; causes swimmer's ear, septicemia, pneumonia, wound infections, conjunctivitis and corneal ulcers, urinary tract infections, CNS infections, folliculitis, and dermatitis; infects any tissue or body site! Also colonizes lungs of cystic fibrosis patients and will remain long-term; results in episodes of breathing problems and a biofilm
    • Diagnosis: Non-fastidious, so they grow on MacConkey agar; produces pyocyanin (blue pigment), pyoverdin (yellow pigmented siderophore), and pyorubrum (red); colonies have green pigmentation with grape-like odor
    • Transmission: Environmental organism that's found in soil, water, and on plant materials everywhere
    • Virulence Factors: Adhesins, exotoxin A, cytotoxins, elastase, phospholipase C, alkaline protease, rhamnolipid, polysaccharide capsule, and antibiotic resistance; slime layer is anti-phagocytic; both our non-specific and specific immune systems defend us against this organism
    • Treatment and Prevention: In CF patients, is difficult to treat; forms biofilms and has many antibiotic resistance genes; combination of drugs
  29. Burkholderia cepacia
    • Description: Very similar to Pseudomonas aeruginosa; gram-negative rod, motile, non-fermentative, non-fastidious, multiple antibiotic resistances
    • Oxygen: Aerobe
    • Oxidase: Positive
    • Catalase:
    • Clinical:
    • Diagnosis: Same as P. aeruginosa in presentation, but it has a lack of pigments and does not produce mucoid colonies
    • Transmission:
    • Virulence Factors: Little is known about pathogenesis beyond the ability to form biofilms in the lungs of cystic fibrosis patients (co-infection with P. aeroginosa)
    • Treatment and Prevention: Poor prognosis and limited therapeutic options--antibiotics are available
  30. Burkholderia mallei and B. pseudomallei
    • Agents of bioterrorism
    • Cause pain in chest, bones, or joints; cough; skin infections; lung nodules; and pneumonia
    • 20-60% fatal even with therapy
  31. Stenotrophomonas maltophila
    • Description: Very similar to Pseudomonas aeruginosa; gram-negative rod, non-fastidious; multiple antibiotic resistances
    • Oxygen: Aerobe
    • Oxidase: Negative
    • Clinical: Known for outbreaks in the hospital setting arising from a variety of contaminated fluids and human colonization; long-term broad-spectrum antibiotics and impaired host defense are risk factors
    • Diagnosis:
    • Transmission: Disinfectant solutions, ice machines, and respiratory equipment
    • Virulence Factors:
    • Treatment and Prevention: Antibiotic sensitivity testing
  32. Acinetobacter baumannii
    • Description: Similar to S. maltophilia and P. aeruginosa; gram-negative, non-motile rod that is fat and coccobacillus-like
    • Oxygen: Strict aerobe
    • Oxidase: Negative
    • Catalase:
    • Clinical: Can colonize any area of skin; called the "Gram-Negative MRSA"; soldiers returning from Iraq/Afghanistan often colonized
    • Diagnosis:
    • Transmission:
    • Virulence Factors:
    • Treatment and Prevention: Specific therapy according to antibiotic susceptibility
  33. Diseases of opportunistic gram-negative rods
    • Bacteremia: Often the result after Pseudomonas aeruginosa, Burkholderia cepacia, Stenotrophomonas, or Acinetobacter gains bloodstream access via wounds, burns, or invasive devices
    • Ecythema gangrenosum: Lesions that can occur in severely neutropenic patients
    • Lung infections: Patients on ventilators
    • UTIs: Patients on urinary catheters
    • Cystic Fibrosis Patients: Significant destruction of lung tissue from P. aeruginosa or B. cepacia
  34. Clues to anaerobic infections
    • Found next to mucosal surface where they reside
    • Form abscesses or areas of tissue necrosis
    • Putrid odor from fermentation products with lots of gas
    • Strict anaerobes like to co-infect with facultative anaerobes, because the latter help get rid of the O2 supply
    • Remember, they won't grow in aerobic culture
  35. Most commonly seen aerobes
    • Gram-Negative Rods
    • Bacteroides fragilis
    • Pigemented Prevotella
    • Non-pigmented Prevotella
    • Porphyromonas
    • Fusobacterium
    • Gram Positives
    • Peptostreptococcus (cocci)
    • Clostridium (long rods, spore formers)
    • Propionibacterium
    • Eubacterium
    • Actinomyces (filamentous)
  36. Clostridium
    • Description: Gram-positive rods; spore-formers which can be central or terminal
    • Oxygen: Anaerobic
    • Oxidase:
    • Clinical:
    • Diagnosis:
    • Transmission:
    • Virulence Factors:
    • Treatment and Prevention:
  37. Clostridium perfringens
    • Description: Gram-positive, large, rectangular rods; non-motile; rarely forms spores which are subterminal
    • Oxygen: Anaerobic
    • Oxidase:
    • Clinical: Causes soft tissue infections, based upon the route of entry; cellulitis is gas formation in soft tissue, no toxemia (dermis infected); fasciitis or suppurative myositis is accumulation of gas and pus in the muscle; myonecrosis is gas gangrene or necrotizing fasciitis (80% of the cases are caused by C. perfringens) with accompanying destruction of muscle and toxemia; anaerobic puerperal sepsis/abortions
    • Can also cause food poisoning via contamination of meat by spores; symptoms come from enterotoxin and include watery diarrhea and crampy abdominal pain within 8-24 hours post ingestion, no fever, nausea, or vomiting, and stools are foamy and foul smelling
    • Diagnosis: Appearance of wound and foul smell; smear shows large gram-positive rods and usually no spores; has a double zone of hemolysis on sheep blood agar; egg yolk agar demonstrates lecithinase by becoming opaque (alpha toxin)
    • Transmission: Found in the intestinal tract of humans and animals, vaginal vaults or crevices, and spores are in the soil and water
    • Virulence Factors: "Major lethal" exotoxins of types A through E (next card); heat-labile enterotoxin encoded for by cpe gene; collagenase (degrades collagen, allowing penetration deeper into tissues and fulminating gangrene); 
    • Treatment and Prevention: >40% mortality with myonecrosis; debride wounds, give hyperbaric oxygen, and antibiotics and antibodies to alpha-toxin; the most difficult part is getting the antibiotics to the site of infection; if ill from food poisoning, need no antibiotic treatment and provide symptomatic treatment
    • Pig-bel necrotizing enteritis: Rare and more severe than above; beta toxin is responsible; is a fatal disease due to acute necrosis in jejunum
  38. Clostridium perfringens "major lethal" toxins
    • Alpha: Most important, produced by all 5 types; is a lecithinase which cleaves lecithin in the membranes of many different kinds of cells; results in massive hemolysis, increased vascular permeability, bleeding, tissue destruction, hepatic toxicity, and myocardial dysfunction
    • Beta: Cuases intestinal stasis and necrotizing enteritis (pig-bel)
    • Epsilon: Increases vascular permeability of the gastrointestinal wall
    • Iota: Necrotic activity and increases vascular permeability
  39. Clostridium difficile
    • Description: Gram-positive rods; forms spores centrally;
    • Oxygen: Anaerobic
    • Oxidase:
    • Clinical: Causes non-bloody diarrhea to life-threatening pseudomembraneous colitis; the pseudomembrane is from inflammation resulting in a PMN influx combined with cellular death; fever and abdominal cramping; associated with prior use of antibiotics that suppress normal flora (normally an endogenous infection)
    • Diagnosis: Is normal GI flora in 2% of general population and 30% of hospitalized patients; isolate in feces or test for toxins to detect; treat with antibiotics (relapses can occur since spores are not killed), possible surgical repair, and stool transplant
    • Transmission: Personal contact; limit transmission by using antiseptic-impregnated soap
    • Virulence Factors: Enterotoxin (Toxin A) stimulates infiltration of neutrophils into the descending colon to disrupt tight cell-cell junction, causing diarrhea; cytotoxin (Toxin B) glycosylates G proteins that are involved in actin filament polymerization, resulting in loss of cytoskeletal integrity and death of enterocytes; surface layer proteins (SLPs) facilitate binding to intestinal epithelium; a hypervirulent strain produces increased levels of Toxins A and B as well as an extra toxin called "binary toxin"
    • Treatment and Prevention:
  40. Clostridium tetani
    • Description: Large, rectangular, gram-positive rods; forms round terminal spores; 40 cases per year in U.S., 1 million worldwide
    • Oxygen: Anaerobic (extremely oxygen sensitive)
    • Oxidase:
    • Clinical: Spores enter a wound and germinate in areas of necrosis and poor blood supply; tetanospasmin blocks inhibitory impulses to motor neurons and results in prolonged muscle spasms due to irreversible binding
    • Generalized tetanus (trsimus/lockjaw, drooling, sweating, generalized tonic spasms) causes compromised breathing in a descending pattern (jaw, neck stiffness, difficulty swallowing, abdominal muscle rigidity); 50% mortality rate
    • Localized tetanus involves persistent muscle contraction in the same area as the wound
    • Cephlic tetanus can occur following otitis media and injury to the ear
    • Neonatal sepsis can happen when spores enter via a contaminated umbilicus or circumcision (>90% mortalitiy)
    • Diagnosis: Bacteria are rarely cultured from wounds (since anaerobic) and toxin/antibodies are not detected in patients, so diagnoses made on history and signs
    • Transmission:
    • Virulence Factors: Tetanus toxin (tetanospasmin) which is an A-B type zinc endopeptidase (stops release of inhibitory glycine and GABA neurotransmitters)
    • Treatment and Prevention: TDaP vaccine with booster every 10 years; patients with anaerobic wounds should be boosted; if the patient's history is <3 doses of vaccine, give tetanus toxid and antibiotics for clean, minor wounds; or tetanus toxid and tetanus immune globulin for other wounds
  41. Clostridium botulinum
    • Description: Large, rectangular, gram-positive rods
    • Oxygen: Anaerobic
    • Oxidase:
    • Clinical
    • Foodborne botulism: Intoxication 12-36 hours after ingestion; has nausea, vomiting, bilateral cranial nerve impairment (drooping eyelids, double vision, blurred vision, enlarged/sluggish pupils, difficulty speaking/swallowing), no fever, descending symmetrical paralysis; causes death by respiratory/cardiac failure (10-20%)
    • Flaccid paralysis due to blockage of ACh release
    • Infant botulism: Caused by spores ingested in honey/infant milk powder; constipation, lethargy, mild weakness, followed by floppy stage; usually recover spontaneously, but 2% mortality
    • Wound botulism: Organism grows in wound and elaborates toxin, resulting in illness like foodborne with less prominent symptoms
    • Inhalation: Rapid onset and high mortality rate
    • Diagnosis: Symptoms and past history; mouse protection test; can try to culture anaerobically after heating sample to kill other bacteria; reportable to public health
    • Transmission: Widely found in soil and water worldwide
    • Virulence Factors: Seven antigenic types of botulium neurotoxin (A-G), which is the most lethal toxin known (.1ug/human is lethal), which can be inactivated by boiling for several minutes (heat labile); botulinum neurotoxin blocks ACh neurotransmission at synapses
    • Toxin also used for: Botox, foot deformities, spasticity, tennis elbow, hemorrhoids; potential for bioterrorism
    • Treatment and Prevention: For intoxication, provide ventilatory support, gastric lavage, antibiotics, and trivalent botulinum antitoxin; prevent by heating food appropriately; vaccine does exist but is not used since disease is so rare
  42. Other Clostridum species
    • C. septicum
    • C. sordellii
    • C. tertium
    • C. novyi: IUD infections; produces anti-tumor effects in experimental animals when toxin gene is removed
  43. Gram-negative non-spore-forming anaerobes
    • Rods
    • Bacteroides
    • Prevotella
    • Porphyromonas
    • Fusobacterium (tapered ends)
    • Cocci
    • Veillonella
  44. Gram-positive non-spore-forming anaerobes
    • Cocci
    • Peptostreptococcus
    • Anaerococcus
    • Rods
    • Actinomyces
    • Propionibacterium
    • Lactobacillus
  45. Bacteroides
    • Description: Gram-negative rods, but are very pleomorphic in size and shape; dark- and light-staining areas within a cell and swollen areas that look like vacuoles can be mistaken as endospores
    • Oxygen: Strict anaerobe
    • Oxidase:
    • Clinical: Major constituent of human colon/feces, oral cavity, and female genital tract; competes with opportunists such as Salmonella and Shigella for nutrients; also provides energy supply of colonic mucosal epithelial cells, vitamin K, and folate; is a problem when extra-colonic
    • Forms abscesses allowing for polymicrobic infections (E. coli often utilizes extra oxygen) in abdomen usually; the most common anaerobic infection after abdominal surgery; also causes diverticulae
    • Can also cause bacteremia, endocarditis, decubitus ulcers (pressure sores), gangrene, cellulitis, and necrotizing fasciitis
    • Diagnosis: Gram stain, colony morphology, anaerobic culture on bile-esculin agar and gentamicin (appears black)
    • Transmission:
    • Virulence Factors: Hyalronidase and neuramidase aid in invasion; large polysaccharide capsule; little or no endotoxin activity due to different structure of LPS
    • Treatment and Prevention: Antibiotics
  46. Prevotella
    • Description: Pigmented gram-negative rods;
    • Oxygen: Anaerobic
    • Oxidase:
    • Clinical: P. gingivalis is a key pathogen in adult periodontitis; infections of Prevotella in general include head, neck, and lower respiratory tract from oral/dental infections and bite infections; lung abscesses; PID, tubo-ovarian abscesses
    • Diagnosis: Produce brown-black pigment on blood agar due to heme protoporphyrin; usually found in polymicrobial infections
    • Transmission:
    • Virulence Factors:
    • Treatment and Prevention:
  47. Porphyromonas
    • Description: Gram-negative rods
    • Oxygen: Anaerobic
    • Oxidase:
    • Clinical: Causes female genital tract, oral, and pulmonary infections
    • Diagnosis: Non-pigmented colonies
    • Transmission:
    • Virulence Factors:
    • Treatment and Prevention: Vancomycin sensitive, whereas Prevotella is vancomycin resistant
  48. Fusobacterium
    • Description: Gram-negative rods with tapered ends
    • Oxygen: Anaerobic
    • Clinical: Found in GI, genitourinary tract, upper respiratory tract, and oral cavity
    • F. nucleatum: Most commonly encountered; causes female genital tract, oral, and pulmonary infections (just like Prevotella/Porphyromonas)
    • F. necrophorum: Very virulent; causes peritonsillar abscesses or Lemierre's syndrome (septic thrombophlebitis of internal jugullar vein following upper respiratory infection that presents with fever and lateral neck tenderness)
  49. Veillonella
    • Description: Most commonly isolated gram-negative anaerobic cocci
    • Oxygen: Anaerobic
    • Clinical: Causes the same infections as gram-negative anaerobic rods--oral, head/neck, and soft tissue infections
    • Diagnosis: Transmission: Virulence Factors: Treatment and Prevention:
  50. Peptostreptococcus
    • Description: Gram-positive cocci; easily decolorized in a gram stain; very variable in size and shape
    • Oxygen: Anaerobic
    • Clinical: Normal flora of skin and mucous membranes; frequently found in mixed infections such as head/neck, intra-abdominal, and pleuropulmonary infections and cellulitis; can cause necrotizing pneumonia if aspirated; bacteremia commonly follows OB/GYN infections and is rarely fatal
    • Diagnosis: Very difficult and slow growing; contamination of clinical specimen with anaerobic cocci that colonize the skin and mucosal surface
  51. Actinomyces israelii
    • Description: Gram-positive rods that appear similar to a fungus
    • Oxygen: Anaerobic
    • Clinical: Normal flora of mucosal surfaces; causes chronic granulomatous lesions, abscesses, and draining sinuses; oral infections are most common (dental-implant-associated infections) and appear as "lumpy jaw"; poor oral hygiene, oral therapy, and IUDs are risk factors; also causes pulmonary (after aspiration), abdominal (after surgery/trauma to bowel), and pelvic (IUD complications) infections or infections of bite wounds (is part of biofilm)
    • Diagnosis: Sulfur granules present; look like molar tooth-like colonies; tough to diagnose due to contamination with normal flora Actinomyces
    • Transmission: Endogenous infections with no person-to-person spread
    • Virulence Factors:
    • Treatment and Prevention: Drainage of abscess, surgical debridement; treatment with antibiotics; good oral hygiene is prevention
  52. Propionibacterium
    • Description: Gram-positive rods, but are very pleomorphic; can look like beads, long rods, etc
    • Oxygen: Anaerobic
    • Clinical: Normal flora of skin, conjunctiva, ear, intestine, female genital tract, mouth--everywhere!
    • Propionicaterium acnes: Causative agent of acne; unrelated to skin cleansing as it develops in sebaceous follicles
    • Treatment and Prevention: P. acnes treated by benzoyl peroxide and antibiotics
  53. Lactobacillus
    • Description: Gram-positive rods
    • Oxygen: Microaerophilic
    • Clinical: Rarely pathogenic; major members of normal flora of female genital tract (lactic acid wase product maintains low pH of normal adult female genital tract)
    • Diagnosis: Not needed
  54. Mycobacterium tuberculosis complex (MTB complex)
    • This complex includes M. bovis (transmitted to us from livestock) and a whole bunch of others
    • 1/3rd of world's population is currently infected!
    • Description: Acid-fast, meaning acid is used as decolorizing agent following heat and dye; rods; unique cell wall (high-lipid, waxy; difficult to penetrate; glycolipid/mycolic acid residues on top of small peptidoglycan layer); intracellular and extracellular
    • Oxygen: Aerobic to anaerobic
    • Clinical
    • Pumonary disease; causes meningitis in children under 5yo; causes extrapulmonary infections of joints, boine, urinary tract, central nervous system, muscles, bone marrow, and lymphatic system; miliary TB is when it's in multiple organs (often fatal)
    • Symptoms: Cough >3 weeks, chest pain, hemoptysis
    • Diagnosis: Tuberculin Skin Test (TST/PPD/Mantoux method) read 48-72 hours after injection (remember that there are lots of false positives and negatives--non-reactor, recent infection, very young age, anergy); acid-fast microscopy of sputum (Ziehl Neelsen is when they look red against blue, Fluorochrome is where they glow); chest X-ray; sputum culture on solid or liquid medium with antibiotics to kill other bacteria (do 3 times at least); nucleic acid testing; latent diagnosis is done via interferon-gamma release assays
    • Transmission: Mycobacterium tuberculosis is an obligate human pathogen; after inhalation, 10% develop disease (infectious dose is 10 cells!)
    • Virulence Factors:
    • Pathogenesis: Inhalation; phagocytosis by alveolar macrophages; inflammatory cell recruitment; chronic cytokine stimulation results in granuloma formation with infected macrophages inside controlling TB spread; outer wall contains fibroblasts, lymphocytes, and neutrophils; calcification; damage of nearby bronchi can allow for spread of TB to other areas and reactivation of disease
    • Treatment and Prevention: Those with a decline in immune system (HIV/AIDS, malnutrition, infection with other diseases, age) or host genetic factors (COPD/impaired lung function) are more likely to progress to TB disease; treatment is 6 months with 4 drugs; prevention is by the bacille Calmette-Guerin (BCG) vaccine
  55. HIV/AIDS and Tuberculosis
    • Immunosuppression induced by HIV modifies the clinical presentation of TB--subnormal clinical presentation, high rate of drug resistance, atypical chest X-ray, TST anergy
    • Only rule out TB in HIV/AIDS patients if they do not have a cough, fever, or night sweats
  56. Drug-resistant tuberculosis
    • Multidrug-resistant and extensively-drug-resistant TB are becoming more common
    • Primary drug resistance is when patient is infected with TB that is already resistant
    • Secondary is when patient is infected with TB that becomes drug resistant over course of infection (due to noncompliance usually)
  57. Mycobacterium leprae
    • Description: Acid-fast rod
    • Oxygen:
    • Oxidase:
    • Clinical: Infection of skin, peripheral nerves (loss of sensation), upper respiratory tract, and eyes; skin lesions may form years later; survive in macrophages and striated muscle, glial cells, and Schwann cells; our immune response is what kills nerve cells
    • There are two types of damage, and they are determined by our immune system (cell/humoral response) to form granulomas or have foamy macrophages
    • Diagnosis: Divides very slowly and cannot be grown in culture; use clinical signs and acid-fast microscopy
    • Transmission: Prolonged contact through droplet transmission (need a lot of bacteria to get sick); risk of disease is NOT impacted by HIV/AIDS; endemic areas are in Africa and Asia; found only in humans, armadillos, and monkeys
    • Virulence Factors:
    • Treatment and Prevention: Multi-drug therapy for 6-12 months
  58. Mycobacterium ulcerans
    • Description: Slow-growing acid-fast rod; extracellular
    • Oxygen:
    • Clinical: Causes Buruli ulcer (first a nodule, then diffuse edema) which is painless and has low mortality; complications include loss of organs such as eye and breast or amputations; 75% of cases are in children under 15yo and frequently causes permanent disability
    • Diagnosis: PCR is most sensitive; can be cultured over 6 weeks
    • Transmission: Has aquatic resorvoir and mode of transmission is unknown
    • Virulence Factors: Mycolactones, which cause the ulcer by necrotizing adipose tissue, causing immunosuppression, and damaging nerves
    • Treatment and Prevention: Antibiotics for 8 weeks and surgery; BCG vaccine may have some immunity
  59. Mycobacterium marinum
    • Description: Acid-fast rod
    • Oxygen:
    • Clinical: Causes opportunistic infections in healthy hosts 2-4 weeks after aquatic trauma; immune suppression can lead to invasive infection/arthritis; similar to M. ulcerans
    • Transmission: Natural host is fish and frogs
  60. Non-tuberculous mycobacteria (NTM)
    • Characterized by Runyon Groups
    • 1: Photochromogens (orange pigment in light; slow-growing)
    • 2: Scotochromogens (orange pigment in light and dark; slow-growing)
    • 3: Nonphotochromogens (non-pigmented; slow growing)
    • 4: Fast growers (colonies form in 1 week or less)
    • The slow growers take 2-6 weeks to form colonies
    • Slow growers: M. avium, M. intracellulare,M. kansasaii
    • Rapid growers: Usually not pathogenic unless in HIV patients
  61. Mycobacterium avium complex (MAC)
    • Description: M. avium and M. intracellulare
    • Clinical: Cause pulmonary infections in patiets with pre-existing conditions (immunocompromised); lymph node abscesses
    • Diagnosis: Based upon where symptoms are (bronchoalveolar lavage, sputum culture, gastric lavage, CSF/blood cultures, wound exudates)
    • Transmission: Infection from water; no person-to-person spread
  62. How to speciate mycobacteria
    Biochemical tests, molecular probes, DNA sequence analysis, mass spectrophotometry
  63. How to treat NTM infections
    • Many are resistant to antituberculosis drugs
    • Surgical resection
    • No vaccine available
  64. Nocardia
    • Description: Long, branching, gram-positive rods; N. asteroides is most common species
    • Oxygen: Aerobic
    • Oxidase:
    • Clinical: Opportunistic infections of severely immunocompromised patients; cellulitis, pulmonary infection, disseminated disease, or brain abscess; 10-40% fatal
    • Diagnosis: Gram stain, specialized culture media, molecular methods; when they show up, it might be due to lab contamination or colonization
    • Transmission: Found in soil, water, and on organic material (decaying)
    • Virulence Factors:
    • Treatment and Prevention: Antibiotic resistance is increasing; combination drug therapy
  65. Legionella pneumophila
    • Description: Gram-negative, rod-shaped bacteria; stain faintly; opportunistic pathogen in immunocompromised, smokers, people over 50, or people who have travelled recently; many species in Legionella and Legionella-like amoebal pathogens (LLAP) are grouped with
    • Oxygen:
    • Oxidase:
    • Clinical: Legionnaires' disease has fever, myalgia, cough, and atypical pneumonia (5-30% fatal); Pontiac fever is a self-limiting, non-fatal respiratory infection; big problem for nosocomial infections due to high number of ill patients and safety measures to prevent scalding from water
    • Diagnosis: Look like ground glass on BYCE media; need culture plus urine antigens and PCR to detrmine if present
    • Transmission: Found in aquatic environments, plus potting soil; is intracellular in amoeba and protozoans naturally, but exists in biofilms also in manmade reservoirs like cooling towers, water distribution systems, or spas; acquired from environment (no human-to-human spread) by inhalation/aspiration
    • Virulence Factors: Evades water treatment and becomes more virulent after growth in amoeba
    • Treatment and Prevention: Antibiotics that reach high intracellular concentrations; decontamination by superheat and flush, filtration, or biocide technologies

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