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192 Cards in this Set
- Front
- Back
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What is the largest family of medically important gram - rods?
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enteric bacteria
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Enteric bacteria - how do they survive?
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faculative anaerobes that ferment glucose
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Enteric bacteria - catalase and oxidase?
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Catalase positive
Oxidase negative |
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What are the most significant pathogenic genera in enterobacteriaceae?
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Escherichia
Klebsiella Proteus Salmonella Shigella Yersinia |
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Describe the virulence of enteric bacteria.
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Endotoxin: lipid A protion of LPS in wall
Capsule: protects against phagocytosis Type II secretion systems: "molecular syringes" that inject virulence factors into target cells Drug resistance: common among enteric bacteria; usually transferred on plasmids |
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Epidemiology of E. Coli
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abundant in GI tract
Most strains cause disease that ahve spricifc virulence factors (typically coded on plasmids, pathogenicity islands, or lysogenic pahge) MOST FREQUENT CAUSE OF GRAM NEGATIVE SEPSIS Cause of >80% of community acquired UTIs and many nosocomial UTIs |
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How many groups of E.coli cause gastroenteritis?
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Five
ETEC EPEC EAEC EHEC EIEC |
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What causes travelers diarrhea?
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ETEC (enterotocigenic E. Coli)
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How is ETEC transmitted?
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indirect fecal oral route (through consumption of fecally contaminated food or water)
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What are the symptoms of ETEC?
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Incubation period: 1-2 days
Watery diarrhea and abdominal cramps common (self limiting within 3 days) Possible dehydration nausea and vomiting less common Non-inflammatory (no inflammatory cells, blood or mucus in stool) and afebrile. -- this points to a toxin and NOT INVASIVE INFECTION |
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What are the two ETEC toxins?
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Heat labile toxin LT-I
Heat Stable toxin Sta |
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What is heat labile toxin LT-1
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toxin of ETEC
A-B exotoxin similar to cholera toxin but less potent Causes increase in levels of intracellular cAMP, which causes hypersecretion of fluids and diarrhea |
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What is heat stable toxin Sta?
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Toxin of ETEC
Monomeric peptide causes increases in levels of intraceullar cGMP which causes hypersecretion of fluids and diarrhea. |
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Symptoms of EHEC?
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Incubation period: 3-4 days
Initial symptoms: non-bloody diarrhea and abdominal pain (+vomiting in about 50% of cases) Within 2 days: bloody diarrhea and severe abdominal pain (hemorrhagic colitis - tissue damage) Resolution in 4-10 days i nuntreated patients |
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What is the Shiga-Toxin-Producing E.coli strain?
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EHEC aka STEC
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What is Hemolytic Uremic Syndrome (HUS)? what is it caused by?
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Caused by EHEC/STEC
Develops 2-14 days after diarrhea starts Symptoms: acute renal failure, thrombocytopenia and microangiopathic anema Usually resolves in 4-10 days but has a 3-5% mortality rate with proper treatment including dialysis Sequelae (permanent after effects): renal impairment, CNS manifestations (encephalopathy), hypertension. |
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Describe Shiga Toxin.
Acquired? Mechanism? |
(STX-1, STX-2)
Acquired by infection with lysogenic bacteriophage. A-B exotoxin (1A subunit and 5 B subunits) B subunits bind to glycolipid that is especially abundant on intestinal villus and renal epi cells A subunit enters cell and is cleared. A1 fragment binds to 28S rRNA and blocks protein synthesis (interferes with ribo function.) Most HUS cases associated with STX-2 |
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What is the most frequent cause of E.coli gastroenteritis cases originating in US?
What is the most common strain? Transmission? |
EHEC/STEC
Strain O157:H7 Mostly by ingestion of food or water contaminated with animal manure Secondary spread by person-to-person transmission |
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What does EAEC cause?
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Cause of persistent watery diarrhea and dehydration in infants in developing countries and travelers.
Might also be important cause of childhood diarrhea in developed countries. |
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What is the most frequent extraintestinal E.Coli disease?
How does it manifest? What are the strains that are most likely cause the most severe infection? |
UTIs
Ascending infections (bacteria from colon --> urethrea --> bladder and possibly --> kidney or prostate) Strains that adhere to uroepi cells more likely to cause kidney prostate infections. |
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What is cystitis?
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most commonly caused by E.Coli
Dysuria, frequency, suprapubic pain More frequent in women |
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What is pyelonephritis?
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Kidney infection caused by E.coli
symptoms of cystitis and fever and back pain Can take take 5-7 days to resolve with proper treatment |
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What is the second most frequent extraintestinal E.coli infection?
Other E.coli infections? |
abdominal and pelvic infections
Include: peritonitis, diverticulitis, appendicitis, visceral abscesses (liver, pancreas, or spleen), cholangitis. Others: Cellulitis Musculoskeletal pneumonia can infect nearly every organ and anatomic site, depending on circumstances |
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What are the two leading causes of neonatal meningitis?
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E.Coli and Group B streptococci
Rare after first month of life |
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What gives you bacteremia and sepsis?
Where does it arise from? |
E.coli
Often arises from UTI or intestinal perforation High mortality in compromised patients |
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What are the general properties of pseudomonas?
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Non-fermentative and OXIDASE POSITIVE
Extremely widespread in nature (can live almost anywhere, including hospitals) It has simple growth requirements and nutritionally versatile Primarily opportunistic pathogens |
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P.aeruginosa virulence factors?
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Adhesions: flagella, pili, LPS
Capsule: protects against phagocytosis and antibios Antibio resistance: many strains have resistance or multiple resistance which make them very hard to treat. LasA and LasB: enzymes that degrade elastin. |
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What are LasB and LasA?
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virulence factors of P.aeruginosa
Damage elastin containing tissues Cause hemorrhagic lesions (ecthyma gangrenosum) that develop in disseminated infections |
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What causes ecthyma gangrenosum?
What is it? |
P.aeruginosa
Hemorrhagic lesions that develop in disseminated infections |
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Major disease of P. aeruginosa?
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Pulmonary
Asymptomatic colonization leads to necrotizing broncho-pneumonia Colonization mostly in pts with cystic fibrosis and other chronic lung diseases or neutropenia Invasive disease in immunocompromised patients |
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What are some skin and soft tissue infections that P. aeruginosa causes?
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Burn wound infections
Folliculitis: from immersion in water Fingernail infections: immersion in water (nail salon) Osteocondritis of foot after penetrating injury |
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Can P. aeruginosa cause UTIs?
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Yes, but they are usually nosocomial and associated primarily with indwelling catheters and/or multiple courses of antibios
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What kind of infection can P. aeruginosa cause in the eye?
Ear? |
Eye: following injury to cornea; corneal ulcers lead to eye-threatening disease
Ear: External otitis (swimmer's ear) or malignant external otitis (invades underlying tissues and affect cranial nerves, bones) |
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How can you get bacteremia and sepsis from P. aeruginosa?
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From infections of lower respiratory tract, urinary tract, or skin/soft tissue infections (especially burn infections)
Occurs most often in patients who are compromised Sometimes can lead to ecthyma gangrenosum Relatively high mortality rate |
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Properties of haemophilus?
What are the most clinically important species? |
Small, pleomorphic, gram-negative rods, commonly on mucus membranes of humans.
Very weird growth requirements Most important: H. Influenzae: superpathogen H.aegypticus: conjuntivitis H. ducreyi: STD (chanchroid) H. parainfluenzae --> bacteremia leading to endocarditis |
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What are the two distinct types of H. influenzae?
What are the virulence factors? |
Nonencapsulated H. Influenzae - low virulence
Type B (encapsulated) - high virulence Adhesions: pili and other surface proteins (colonization of oropharynx) LPS and glycopeptide in cell wall: damage epithelium, facilitate movement --> epi and endo cells and entry into bloodstream (mostly type b) Polyribitol phosphate (PRP) capsule (type b only): prevents phagocytosis |
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What are some diseases that H. Influenzae type B can cause:
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Meningitis (pediatric, but there is a vaccine now)
Epiglottitis (celulitis and swelling) Cellulitis - reddish blue patches on periorbital area of cheeks (vaccine) Arthritis; infection of single large joint secondary to bacterima (mostly pediatric before vaccine) |
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What are some diseases that nonencapsulated H. influenzae causes?
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Sinusitis and otitis media: acute and chronic forms most often caused by H. influenzae or S. penumoniae
Lower respiratory disease: in pts with chronic pulmonary disease |
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What are some opportunistic gram negative rod diseases?
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Respiratory infections
Periodontal disease Bran abscesses Intraabdominal infections Gynecologic infections Skin and soft tissue infections Bacteremia Gastroenteritis |
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Properties of the Human herpes viruse?
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Large, enveloped viruses with DOUBLE STRANDED DNA genomes and icosadeltahedral capsids
Infections very common Usually cause benign diseases, but some infections --> significant morbidity and mortality, especially in imunocompromised patients 8 types (HHV1-HHV8) |
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Describe the pathogenesis of HSV-1 and HSV-2.
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1. Infections --> mucuous membranes or breaks in skin
HSV 1 - usually infects above waist HSV 2 - usually infects below waist 2. Replication (lytic infection) in mucoepi cells -Cell death from degradation of host cell DNA, inhibition of host cell macromolecular synthesis - Viral damage to tissues and inflammatory and cell mediated responses --> vesicular lesions and other symptoms -Lesions usually heal without scarring 3. Establishment of latent infection in neurons - infects neuron innervating initial site of active infection and travels to trigeminal ganglia (oral herpes) or sacra gangia (genital) - in neruons, one small region of viral genome transcribed, generates LATENCY ASSOCIATED TRANSCRIPTS (not transcribed into proteins and viral replication cycle does not proceed) - no detectable cell/damage from latent infection 4. Reactivation of infection --> recurreances - stimuli that may activate virus: stress, trauma, exposure to sunlight - virus replicates in single nerve and travels down nerve to mucoepi surface - active replication (lytic infection) in mucoepi cells --> recurrence of lesions |
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Host responses of HSV1 and HSV2.
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Innate responses (interferon, NK cells) can limit progression of initial infection
T helper associated and CD8 killer T cells responses REQUIRED to kill infected host cells and RESOLVE active infection Antibody responses neutralize extracellular viruses (limiting spread) but cannot RESOLVE active infection Combined defenses cannot resolve latent infections |
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How are HSV-1 and HSV2 transmitted?
How is infection site determined? |
vesicle fluid, saliva, vaginal secretiosn, primarily during close contact ("mixing and matching of mucous membranes"
Infection site determined by which membranes mix (both types cause oral and genital lesions) |
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HSV1 and HSV2 lesions
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Typically progress from clear vesicles on reddened base --> pustular lesions --> umbilicated (depressed) ulcers --> crusted lesions
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What is gingivostomatitis? What is it caused by?
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Massive outbreak of cold sores in mouth area
Primarily in young kids or immunocompromised pts Caused by HSV1 or 2 |
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What is herpetic Whitlow?
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INfection of fingers (virus --> break in skin)
Occurs in nurses/physicians attending patients with HSV infections, thumb sucking children, and persons with genital herpes |
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What is herpes gladitorum?
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herpes infection of the body
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What is eczema herpaticum?
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Occurs in children with active eczema - opens skin up for herpes infection
relatively rare in adults underlying disease promotes spread of viral infection |
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Herpetic keratitis?
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typically limited to one eye
Recurrances leads to corneal scarring and damage and possible blindness May be transferred to eye on fingertips from oral or genital infection |
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What is herpes encephalitis? WHat strain is it associated with?
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HSV1
Limited to one termproal lobe Destruction of temporal lobe --> RBCs in CSF, seizures and focal neurologic abnormalities Most frequent form of viral sporadic encephalitis (no vector like insect) Significant morbidity and mortality |
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What is herpes meningitis? What strain is it associated with?
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HSV 2
Usually a complication of HSV2 genital infection Self, resolving with minimal mortality |
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What is neonatal herpes?
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Infection occurs in utero, during birth (most often) or postnatally (from family or hospital personnel)
HSV2 --> liver lungs, CNS Infection of CNS --> death, neuro disabilities, or mental retardation |
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General properties of adenoviruses
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Nonenveloped viruses with icosadeltahedral capsids
linear DOUBLE STRANDED DNA |
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What are adenoviruses capable of causing (generally)?
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Lytic infections (mucoepi cells)
Latent Infections (lymphoid, adenoid cells) Transforming infections (in hamsters, not humans) |
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Pathogenesis of adenoviruses
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Initial infection of eye, upper respiratory, or GI epi cells (site of infection determines what kind of infection)
Possible viremia and spread to visceral organs and/or skin Laten infection of lymphoid and other tissues (adenoids, tonsils, Peyer's patches) Latent infections sometimes reactivate in immunocompromised patients) |
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How do the adenoviruses differ from herpes in structure?
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Adeno is nonenveloped and therefore more hardy
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Transmission of adenoviruses?
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aerosols, fingers, fomites, decal-oral route
No animal reservoirs Many asymptomatic infections |
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What are some adenovirus respiratory diseases?
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1. Pharyngitis
2. Pharyngoconjunctival fever 3. acute respiratory disease 4. other respiratory diseases (colds) |
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Adenovirus in the eye causes?
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Conjunctivitis with some hemorrhaging.
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What are the viruses in the Picornavirus family?
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Hepatoviruses (hep A)
Rhinoviruses Enteroviruses that include: - Poli Coxsackie A Coxsackie B Echoviruses |
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Basic properties of the enteroviruses
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Nonenveloped viruses with icosahedral capsids and very small positive sense SINGLE STRAND RNA genome
Capsids highly resistant to harsh environment conditions and toxic substances in human GI tract. Transmitted via decal-oral route, but rarely cause GI diseases Most infections mild or asymptomatic |
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Pathogenesis of enteroviruses
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Portals of entry: upper respiratory tract, oropharynx, and intestinal tract
Initial infection in mucosa, lymphoid tissues of tonsils and pharynx. Later infection of lymphoid cells and Peyer pateches underlying intestinal mucosa Viremia: virus --> reticuloendo cells of lymph nodes, spleen, liver --> secondary amiplifcation Secondary viremia: virus --> ultimate target tissue --> symptoms |
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How are enteroviruses spread?
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Human pathogens
Fecal oral route Asymptomatic shedding of viruses in feces for up to 30 days puts viruses in enviro Coxsackie and echoviruses also spread by respiratory droplets |
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Coxsackievirus/Echovirus Diseases
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Mild upper respiratory and flu like diseases - MOST FREQUENT
Pleurodynia (Bornholm disease, "devils grip") Herpangina Hand-foot-and-mouth disease Myocarditis and pericarditis Viral meningitis Fever, rashes, common colds |
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What is Pleurodynia (Bornholm disease)? What is it caused by?
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Caused by Coxsackie B
Sudden onset of fever and excruciating low thoracic, pleuritic chest pain Muscles on affected side extremely tender Possible vomiting and abdominal pain Resolves after about 4 days (but may relapse) |
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What is herpangina? What is it caused by?
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Caused by Coxsackie A (not related to herpesviruses)
Fever, sore throat, pain on swallowing, anorexia, vomiting Ulcerated lesions around soft palate and uvula Self limiting |
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What is hand-foot-mouth disease? What is caused by?
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Caused by coxsackievirus A16
Vesicular lesions on hands, feet, mouth, and tongue Self resolves |
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What is bordetella?
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A small strictly aerobic, gram negative coccobacilli
Four species that infect humans: - B. pertussis (whooping cough - pertussis) - B parapertussis: mild pertussis - B. bronchiseptica: respiratory infections (rare) - B. holmesii: sepsis (rare) |
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Virulence and pathogenesis of B. pertussis?
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Adhesions: facilitate attachment in respiratory tract
Pertussis toxin: increased production of mucus and respiratory secretions Tracheal cytotoxin: damages/kills ciliated cells - disrupts clearance mechanism in upper respiratory tract - with excess mucus production as a result of the infection leads to characteristic pertussis paroxysmal cough |
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Epidemiology of B. pertussis
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Transmission via respiratory droplets
No animal reservoirs |
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What causes whooping cough?
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B. pertussis
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What are the characteristics of whooping cough? (incubation stage, catarrhal stage, paroxysmal stage)
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Incubation: 7-10 days (asympto)
Catarrhal stage: 1-2 weeks (cold like symptoms with very high risk of transmission) Paroxysmal stage: 2-4 weeks. Series of repetitive coughs usually followed by characteristic "whoop" sound on inspiration. This results as airway constriction from mucus accumulation. Paroxysms (up tp 50/day) often lead to vomiting, exhaustion. |
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What is the last stage of whooping cough?
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Convalescent stage: 3-4 weeks
Paroxyms diminish in frequency and severity Secondary complications possible (viral infections) |
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What is corynebacterium?
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Aerobic or facultative, gram +, coryneform (irregular, club shaped) rods
Normal colonizers of skin and mucous membranes (several opportunistic species) |
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What is the most important human pathogen species of corynebacterium?
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C. diphtheriae
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What is virulence factor of C. diphtheriae?
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diphtheria toxin
produced at the sight of infection and goes to bloodstream (produces systemic effects of diphtheria) |
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What is the diphtheria toxin coded for by?
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tox gene from lysogenic phage (b-phage)
Classic A-B exotoxin |
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Describe the structure of the diphtheria toxin
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B subunit binds to heparin-binding epidermal growth factor (on many types of Euk cells, especially in HEART AND NERVE cells)
A subunit inactivates elongation factor 2 required for movement of growing peptide chain on ribosome. Net effect of toxin: stops protein synthesis which leads to death of target cell. |
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Epidemiology of C. diphtheriae
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Occurs worldwide
Human pathogen with no known animal reservoirs maintained by asymptomatic carriage in oropharynx and/or on skin of immunocompromised individuals Transmission: respiratory droplets Virtually eliminated in US |
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Describe Respiratory Diphtheria
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Incubation period: 2-4 days
Sudden onset of malaise, low grade fever, exudative pharyngitis, sore throat - bacteria grows on epitheial surfaces in thrat area - exotoxin --. localized cell/tissue damage Development of thick PSEUDOMEMBRANE - dirty grey, leathery looking layer of material covering tonsils, uvula, palate - adheres firmly to underlying tissues - membrane eventually dislodges on its own (expectorated) |
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What is a unique symptom of respiratory diphtheria?
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- dirty, gray, leathery looking layer of material covering tonsils, uvula, palate
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What can severe cases of respiratory diphtheria lead to?
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Systemic symptoms (from toxin)
Myocarditis which can lead to CHF, arrhythmias, death Neuropathy: initially in soft palate and pharynx, but later --> oculomotor and ciliary paralysis --> peripheral neuritis |
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What are the "typical" community acquired pneumonias?
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Strep pneumoniae (most likely)
Haemophilus influenzae Morazella catarrhalis Oral anaerobes (porphyromonas, prevotella) |
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What are the "atypical community acquired pneumonias?
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legionella pneumophila
mycoplasma penumoniae chlamydophila pneumoniae |
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What are the hospital acquired (nosocomial) pneumonias?
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Gram negative rods: most likely (enteric bacteria and P. aeruginosa)
Staph aureus Oral anaerobes |
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What is legionella?
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Slender, pleomorphic, GRAM NEGATIVE ROD
Do not stain with usual reagents in clinical specimens |
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What is the most important Legionella pathogen?
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L. pneumophila
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What is the pathogenesis of L. pneumophila?
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facultattive intraceullar parasite; replicates in alveolar macrophages, monocytes and alveolar epi cells
Bacteria ingested, but prevents phagolysosome fusion, replicates and eventually kills cell Infected macros release cytokines --> strong inflammatory response. |
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What is the epidemiology of L. pneumophila?
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Common habitats: lakes and streams, air conditioning cooling towers and condensers, water systems (shower heads, hot tubs)
Humans infected from environment via inhalation of contaminated aerosols -- NOT TRANSMITTED PERSON TO PERSON 25% of US cases nosocomial (high-risk population) |
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What is Legionnaries Disease caused by? Discuss the progression.
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L. pneumophila
Incubation period: 2-10 days Abrupt onset of fever, chills, headache, and fatigue --> dry, only slightly productive cough and chest pain Primary manifestation: pneumonia often leading to multilobar consolidation (visible in x-rays) GI symptoms: abdominal pain, nausea, vomiting, and diarrhea Mortality: 15-75% depending on pt status |
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What is mycoplasma? What are the important human pathogens?
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very small pleomorphic bacteria that LACK CELL WALLS
Cell membranes contain steroids Important human pathogens: M. Pneumoniae - primary atypical pneumonia M. genitalium - nongonococcal urethreitis (NGU), PID M. hominis - UTIs, postpartum fever |
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Epidemiology of M. pneumoniae?
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it is a mycoplasma
respiratory disease cocurs world wide and year long Most frequent in school kids Transmission: respiratory droplets, especially among classmates, family members Many infections asymptomatic |
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What causes tracheobronchitis?
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mycoplasma pneumoniae
Most common symptomatic presentation Incubation period: 2-3 weeks (relatively long) Mild fever, malaise, headache, non-productive cough (pharyngitis in some cases) Symptoms worsen and persist for 2 weeks or longer (can be very persistent) |
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What is primary atypical pneumonia caused by?
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M. penumoniae
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What is primary atypical pneumonia? What are some possible complications
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"Walking pneumonia"
Patchy brochopneumonia Chest radiographs typically appear more impressive than would be expected from ausculatation of chest Possible complications: Neurologic abnormalities Pericarditis Hemolytic anemia arthritis mucocutaneous lesions |
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What is chlamydiaceae?
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very small, GRAM NEGATIVE, pleomorphic bacteria
Cell walls lack peptidoglycan layer obligate intracellular parasite Two distinct cell forms: - Elementary body (EB): metabolically INACTIVE, infectious form (resistant to harsh environment factors) - Reticulate body (RB): metabolically ACTIVE, noninfectious form. (fragile, cant survive outside host cell) |
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What is a unique structural element of clamydiaceae?
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lack peptidoglycan layer in cell walls
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What kind of organism is chlamydiaceae?
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obligate intracellular parasite
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What are the human pathogens of chlamydiaceae?
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Chlamydia trachomatis: NGU, trachoma, inclusion conjunctivities, lymphogranuloma venereum
Chlamydophila pneumonia: respiratory diseases Chlamydophila psittaci: psittacosis (orinthosis) |
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Epidemiology of C. pneumoniae?
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Chlamydiaceae
Human pathogen with no known animal reservoirs Peack incidence of initial infections in early adulthood Transmission: probably person to person |
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What are some diseases that are caused by chlamydiaceae pneumoniae?
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Acute respiratory infections: pharyngitis, sinusitis, bronchitis
Atypical pneumonia: similar to mycoplasma pneumonia - fever, non productive cough, mold to moderate illness - can be very severe in elderly patients however MAY be involved with atherosclerosis |
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Epidemilogy of C. psittaci
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Chlamydiaceae
Cause of orinthosis Common pathogen of birds Present in blood and tissues, feathers, feces of infected birds Humans and animals infected by inhalation of contaminated aerosols |
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What is orinthosis? What is it caused by?
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Disease caused by c.psittaci
Also caused by psittacosis Incubation period: 6-14 days Very high fever, severe chills Dry hacking cough, cervical adenopathy, mild sore throat, pharyngitis Some pts have GI symptoms Serious: can lead to CNS involvement --> encephalitis, convulsions, coma, death in untreated cases |
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What is epidemiology?
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formal study of mechanisms/factors involved in appearance/spread of infectious diseases within human population
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What is meant by etiology?
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cause/origin of infectious disease
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What is meant by transmission?
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how a disease is spread
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What is meant by reservoirs of infection?
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any living or nonliving materials in or on which some infectious agent is able to survive, multiply, and develop (and that, as a result, can be a source of disease caused by that agent)
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You check for a pulse and there is none. AED is beside the patient. What is the next step.
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connect the AED and analyze.
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What is meant by recovery period?
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period near end of disease cycle;
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what is meant by a carrier?
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healthy individuals that can transmit disease to others
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What is a passive carrier?
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Release pathogens without ever having any signs or symptoms of disease
Pathogen part of normal floa; host immune to it |
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What is an active carrier?
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release pathogens for a long period of time after fully recovering from infectious disease
Individual no longer infected Pathogen becomes part of normal flora; host gained immunity during disease |
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What is zoonoses?
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diseases that can be transmitted between animals and humans
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What are non-living things primary reservoirs for?
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non-communicable diseases (diseases that are most often acquired directly from environment)
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Name some non-living reservoirs of infection?
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Soil
Water Foods |
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How do most pathogens exit humans?
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secretions
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What is vertical direct contact transmission?
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transmission from parents to offspring
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What is horizontal direct contact transmission?
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most often occurs by kissing, handshaking, contact with sores/wounds, sexual contact.
also occurs as result of poor hygenic practices (direct fecal-oral transmission) |
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What is fomite transmission?
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any inanimate object on which pathogen can survive -- considered indirect contact transmission
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What are some modes of indirect contact transmission?
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Fomites
Droplet |
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What are droplet nuclei?
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droplets that settle dry into droplet nuclei and can be re-suspended in air as dust and inhaled.
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What are some ways of transmission by vehicles?
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airborne
foodborne waterborne |
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what is a vector?
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living organisms that transmit disease from one host to another
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What is a mechanical vector?
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passively transmit pathogens on feet or body; not infected
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What is a biological vector?
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actively transmit pathogens that spend part of life cycle in vector; vector infected by pathogen
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What are three medically important groups of gram positive cocci?
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Aerobic, catalase positive: staph
Aerobic, catalase negative: strep, entero Strictly anaerobic: petostrep |
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Describe staph (gram, shape, metabolism, catalase)
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Gram positive
Cocci Aerobic Catalase positive |
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Describe Strep (gram, shape, metabolism, catalase)
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gram positive
cocci aerobic catalase negative |
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Describe enterococcus (gram, shape, metabolism, catalase)
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gram positive
cocci aerobic catalase negative |
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Describe peptostreptococcus? (gram, shape, metabolism)
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gram positive
cocci strictly anaerobic |
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Is staph aureus coagulase positive or negative?
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positive
ONLY COAGULASE POSITIVE species to infect humans |
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Is Staph epidermidis coagulase positive or negative?
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negative
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Is staph saprophyticus coagulase positive or negative?
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negative
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What are S. aureus's virulence factors associated with cell components?
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capsule/slime layer: inhibits phagocytosis and allows adherence to foreign surfaces
Petidoglycan: stimulates production of pyrogens. Mild endotoxin like activity which leads to cytokine production, activates complement. Also promotes abscess formation Adhesins: teichoic acids and adhesin proteins facilitate binding to molecules on host tissues. MSCRAMM Protein A: binds to Fc receptor of IgG 1, 2, and 4. Prevents antibody mediated clearance of bacteria from site of infection. |
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What is MSCRAMM? what bacteria is it associated with?
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microbial surface components recognizing adhesive matrix molecules
S. aureus |
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What are S. aureus's virulence factors associated with cytotoxins?
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Alpha toxin
Beta toxin (spingomyelinase C) Gamma Toxin Panton-Valentine (P-V) leukicidin Delta toxin ---These lead to membrane damage and lysis/cell death |
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What are S. aureus's virulence factors associated with exfoliative toxins (ETA, ETB)?
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Serine proteases that cleave desmoglein 1
Disrupt intercellular bridges in stratum granulosum epidermis (destabilizes dermis) Cause large areas of skin to peel off Cause symptoms of staphylococcal skin syndrome |
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What aspect of S. aureus's virulence causes SSSS (Ritter's syndrome)?
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Exfoliative toxins (EFA, EFB)
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What causes SSSS (Ritter's Syndrome)?
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S. aureus
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What are S. aureus's virulence factors associated with enterotoxins?
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heat stable and resistant to hydrolysis by GI tract enzymes
mild superantigens: nonspecific stimulation of T cells which cause release of cytokines Diarrhea, vomiting, and nausea Associated with staph food poisoning |
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What are S. aureus's virulence factors associated with toxic shock syndrom toxin?
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(TSST-1)
Strong superantigen (cytokine storm) Leakage or killing of endo cells (depending on concentration) leads to loss of fluid from circulatory system Penetrates mucosal barriers (migrates from site of infection and produces systemic effects) Can result in death from hypovolemic shock which can lead to multiorgan failure |
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What are S. aureus's virulence factors associated with enzymes?
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Coagulase: clumping factor which converts fibrinogen to fibrin
Hyaluronidase: spreading factor which hydrolyzes hyaluronic acid between tissue cells and facilitates the spread of bacteria through tissues. Lipases: hydrolyze lipids which allows survival of pathogen in sebaceous areas and promotes skin infections. |
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What is a coagulase and what pathogen is it a virulence factor for?
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clumping factor which converts fibrinogen to fibrin
probably plays a role in abscess formation. S. aureus |
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What is a hyaluronidase and what pathogen is it a virulence factor for?
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spreading factor which hydrolyzes hyaluronic acid between tissue cells and facilitates the spread of bacteria through tissues.
S. Aureus |
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What are the general factors of virulence for S. aureus?
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Cell components
Cytotoxins Exfoliative toxins Enterotoxins Toxic shock syndrome toxin Enzymes |
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Where does S. aureus colonize?
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oropharynx, nasopharynx, GI tracts, and genitourinary tract
transient colonizer of skin |
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Symptoms of which S. aureus diseases almost solely result from toxin activity?
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Staph scalded skin syndrome
Staph food poisoning toxic shock syndrome |
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What is staphylococcal scalded skin syndrome (Ritter's)? What is it caused by?
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abrupt onset of perioral erythema that spreads over entire body within 2 days
Bullae (large blisters) form, with clear fluid (typical of toxin related disease) Desquamation of epithelium Slight pressure displaces skin (Nikolsky's sign) Most cases related to exfoliative toxin ETB Resolution: 7-10 days with no scarring and occurs most often in neonates and young children may lead to serious secondary bacterial infections caused by S. aureus |
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What is bullous impetigo? what is it caused by?
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Caused by S. aureus
Localized form of SSS, typically arising from S. aureus skin infection Most cases associated with exfoliative toxin ETA Localized bullae that DO contain bacteria No positive Nikolsky's sign Highly communicable |
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Which disease is associated with ETA? Which bacteria?
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S. Aureus
Bullous impetigo |
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Which disease is associated with ETB? Which bacteria?
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S. aureus
SSSS |
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How is food contaminated in Staph food poisoning?
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by humans - sneezing, contaminated fingers
Food must remain at room temp or higher for bacteria to grow and produce toxin not destroyed by cooking |
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What is toxic shock syndrome? What is it caused by?
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Caused by S. aureus' toxin shock toxin
Growth of bacterium in vagina or wound leads to release of toxin into bloodstream Early symptoms: fever, hypotension, diffuse macular erythematous rash Later symptoms: vomiting, diarrhea, ab pain and myalgias. Skin desquamates during convalescence |
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What is non-bullous impetigo? What is it caused by?
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caused by S. aureus
Superficial infection, usually on face and/or limbs Occurs most often in young children Pustular lesions that create thick, honey-colored crusts CAN ALSO BE CAUSED BY STREP PYOGENS |
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What are some minor skin issues that S. aureus can cause?
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Folliculitis
Stye Furuncle (boil): extension of folliculitis Carbuncle (large boil) |
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What mediates the resistance of MRSA to pens?
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mecA gene
One staph cassette chrom SCCmec Codes for modified PBP that is not bound by pens but retains normal activity |
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Where do streptococcus bacterium grow best?
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blood or serum enriched media
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What are the serologic differentiations of streptococcus based on?
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Lancefiled groups A--> W are based on cell wall antigens (carbs)
Some species lack antigens that cant be grouped |
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What are the three classificiations of streptococcus on blood agar?
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Hemolytic patterns
Alpha: partial hemolysis (green) Beta: complete (clear) gamma: none |
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What are the basic characterisitcs of S. pyogenes?
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Streptococcus!
Strongly b-hemolytic cocci Lancefield GROUP A M protein:major type specific protein |
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What is M protein? what pathogen is it associated with?
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Strep pyogene
Major type specific protein Two polypeptide chains complexed in alpha-helix anchored in membrane and extends through cell wall portion inside cell wall highly conserved 2 classes: - class 1: shared exposed antigens - class 2: lack shared exposed antigens binds to beta globulin factor H, which degrades complement component C3b when it binds to cell near M protein. Binds fibrinogen and blocks activation of complement by alternative pathway. |
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What are the virulence factors of S.pyogene associated with mechanisms for avoiding opsonization and phagocytosis?
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Hyaluronic acid capsule: interferes with phago
M protein: binds to beta globulin factor H, which degrades complement component C3b when it binds to cell near M protein. Binds fibrinogen and blocks activation of complement by alternative pathway. C5a peptidase: inactivates complement componenet C5a which is a chemoattractant of neutrophils and mononuclear phagos. Inhibits abscess formation in early stages of infection. |
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S. pyogene virulence factors associated with adherence to and invasion of host cells.
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Strepto!!!
Adherence: - initial weak interaction bw lipoteichoic acid and fatty acid binding sites on fibronection and epi cells - M protein, F protein nad other adhesins interact with host cells to complete adherence process Invasion: - M protein and F protein stimulate cells to internalize bacteria - important for maintaining persistent infections and invasion into deep tissues |
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S. pyogene virulence factors associated with pyrogenic exotoxins?
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SpeA, B, C, F
Superantigens: stimulate macros and T-helpers to secrete proinflammatory cytokines Considered responsible for manifestations of severe streptp diseases and for scarlet fever |
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S. pyogene virulence factors associated with enzymes
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Streptolysins S and O: lyse leuckocytes, erythrocytes, and platelets (streptolysin S --> Beta hemolysis.
Streptokinases A and B: degrade blood clots and fibrin deposits (facilitates spread of bacteria in infected tissues. DNAases A, B, C, and D: depolymerize free DNA in pus (reduces viscosity and facilitates spread of bacteria) |
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What do streptolysins S and O do? What pathogen are they associated with?
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Streptococcus pyogene
lyse leuckocytes, erythrocytes, and platelets (streptolysin S --> Beta hemolysis. |
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What do streptokinases A and B do? What pathogen are they associated with?
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Strep. pyogene
degrade blood clots and fibrin deposits (facilitates spread of bacteria in infected tissues. |
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DNAases A, B, C, and D. What pathogen?
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Strep pyogenes
depolymerize free DNA in pus (reduces ciscosity and facilitates spread of bacteria) |
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What are the general virulence factors of S. pygoenes?
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Mechanisms for avoiding opsonization and phagocytosis
Adherence and invasion of host cells Enzymes pyrogenic exotoxins |
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What is streptococcal pharyngitis? What is it caused by?
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Strep pyogenes
Strep throat Sudden sore throat, fever, malaise, headache Posterior pharynx typically erythematous, often with exudate on tonsils Cervical lymphadenopathy may be prominent mild cases very similar to viral pharyngitis; must use diagnostic test to confirm strep throat |
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What are the diagnostic tests for streptococcal pharyngitis?
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Rapid streptococcal antigen test (throat swab): tests for Lancefield group A antigen
Confirm negative results by culturing throat swab |
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What is scarlet fever? What is it caused by?
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Strep pygenes
Caused by strains carrying lysogenic phage (mediates production of pyrogenic toxin) Diffuse erythematous rash Complication of strep throat |
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What disease is strawberry tongue associated with?
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Scarlet fever caused by strep pyogenes
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What is rheumatic fever and what is it caused by?
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Strep pyogenes
Triggered by specific types of Class 1 M proteins that provoke unusually vigorous antibody response. Heart manifestations: pancarditis, possible chronic, progressive damage to heart valves Inflammatory reactions in joints |
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Why can rheumatic fever affect the heart?
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antibodies to M protein of S pyogenes cross react with heart tissue
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What disease can both S. aureus and S pyogene cause?
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non-bullous impetigo
Strep: pyoderma Staph: non bullous impetigo |
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What is erysipelas?
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S. pyogenes
acute skin infection localized pain, inflammation, lymphadenopathy systemic signs involved skin areas often raised and clearly differentiated |
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What is cellulitis?
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infection of skin and underlying tissues
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What is necrotizing faciitis?
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Strepotococcal gangrene caused by S. pyogenes
Infection of deep subQ tissue that spreads along fascial planes Extensive destriction of muscle and fat Minor cut or trauma --> cellulitis, bullae, gangrene --> toxicity, multiorgan failure --> death Prompt, aggressive surgical debridement of infected tissue necessary to save patient |
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What is the difference between staph toxic shock and strep toxic shock?
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Most pts with strep also have necrotizing fasciitis
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What is acute clomerulonephritis
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acute inflammation of renal glomeruli with edema, hypertension, hematuria, proteinuria
caused by specific nephrogenic strains of S. pyogenes |
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Basic properties of S. pneumoniae
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Cocci in PAIRS (Diplococci) or short chains
alpha-hemolytic on blood agar --> GREEN COLOR No lancefield group Capsule polysaccarides used for serologic grouping of strains |
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S. pneumoniae virulence factors
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colonizes oropharynx; then amy go to lung, middle ear, or paranasal sinuses
Surface adhesin proteins: mediate initial binding to epi cells in oropharynx Virulence factors that can defeat major mechanism that defends sensitive parts of respiratory system (flow of mucus away from sensitive areas) - secretory IgA protease: degrades secretory IGA and prevents binding of bacteria to mucin - Pneumolysin: lyses ciliated epi cells - facilitate migration to lungs, sinuses and middle ear Teichoic acid and petidogylcan fragments: activate alternative complement pathway Avoiding phagocytosis: capsule, pneumolysin, phosphocholine in cell wall |
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How is most damage done by S. pneumoniae?
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host responses rather than by toxins
Teichoic acid and petidoglycan fragments pneumolysin |
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What is pneumolysin? What pathogen is it associated with?
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S. pneumoniae
activates classic complement pathway Production of C3a and C5a --> inflammatory processes cytokines (IL-1, TNF-alpha) produced, stimulate additional inflammatory cells to migrate to site of infection Inflammatory response leads to fever and tissue damage also kills some types of phagocytic cells |
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What is phosphocholine? Pathogen?
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S. pneumoniae
Binds to receptors leukocytes, platelets, endo cells and tissue cells in lungs and meninges allows bacteria to enter cells (protected from phagocytosis and invade bloodstream or CNS |
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What is pneumococcal pneumonia? Pathogen?
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S. pneumoniae
Bacteria grows rapidly in alveolar spaces which causes: - accumulation of erythrocytes, neutrophils, and alveolar macros - consolidation of alveolar spaces often in lower lobes fever, chest pain, blood tinged sputum Resolution requires production of antibodies against capsule polysaccharides |
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Other than pneumonia, what other diseases are associated with S. pneumoniae?
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Sinusitis and otitis media: often follows viral infection of URT
Bacteremia Meningitis |
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What is the most frequent cause of meningitis in adults over age 20?
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S. pneumoniae
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What is the most important anaerobic gram positive cocci?
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peptostreptococcus
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What is the largest family of medically important gram negative rods?
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enteric bacteria
faculative anaerobes that ferment glucose Catalase-positive and virtually all oxidase negative |
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Virulence factors for enterobacteriaceae
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Endotoxin: lipid A potion LPS in wall
Capsule: protects against phagocytosis Type 3 secretion systems: molecular syringes that inject virulence factors into target cells Drug resistance: common among enteric bacteria; usually transferred on plasmids |
