Respiratory Flashcards
Actinomyces israelii
- Pathogen category: G+ filamentous branching rod (fungal appearing), obligate anaerobe, extracellular
- Source: normal oral flora
- Virulence factors: depends on the other bacteria to start infection
- Clinical: dental abscess with draining tracts and sulfur granules (Actinomycosis)
- Immune response: local inflammatory response
- Treatment/Prevention: debridement and penicillin for extended period
Actinomyces israelii: a fungal-appearing Gram positive bacterium with branching filaments that lives in anaerobic corners of the mouth. A low level pathogen that typically has co-infecting bacteria (of which there are many in the mouth!).
Actinomyces- normal floral type thing if it is introduced into trauma tissue developing and when getting established developing fibrosis and taking longer to penetrate into the tissues. Breaking of the tooth and jarring them into tissues and may even have a draining of sinuses. Sulfur granules clumps of cell and fungus like bacteria popping out of those sinuses.
Actinomycosis, as seen here, presents as abscesses (discharged purulence with a “sulfur granule” appearance) with draining sinus tracts. Treat with penicillins for several weeks (“looks like a fungus, treat as long as you would a fungus”).
Bordetella pertussis
- Pathogen category: G- rod, aerobic, extracellular
- Source: human reservoir, spread by respiratory droplets, very contagious
- Virulence: exotoxins assist with adhesion and adenylyl cyclase toxin that interferes with neutrophil function; pertussis toxin (inhibits G protein to lessen PMN activity), hemagglutinin (adhesion), adenylyl cyclase toxin (triggers neutrophil destruction)
- Clinical: pertussis (whooping cough)
- Immune response: antibodies to toxin
- Treatment/Prevention: DTap (acellular pertussis); azithromycin
- Diagnosis: swab from posterior nasopharynx for culture
Bordetella pertussis: pertussis or whooping cough, where paroxysmal coughing is followed by a “whoop” of inspired air past the partially closed airway. Gram negative rod, macrolides indicated for treatment.
Bordatella adhere in the larynx and trachea, adherant professional in respiratory pathogen affecting epithelium producing inflammatory response and developing metaplstic changes. Mucus and bronchial obstruction comon in children. Bronchial obstruction- create barotrauma with the cough lethal to children. If adult have chronic cough consider this as the differential.
Pertussis gives off toxins- toxin activity as it is given off inhibiting G protein to lessen neutrophil from coming into the area and killing off bacterial. Pertussis- hung up as lymphocytosis toxin interferes with high endothelial venules (easy egress into the lymphocytes) making them unable to go through and make up with cognate antigen. Adenylyl cyclase- neutrophils not effectively killing off.
Do a acellular pertussis in the TDAP generating immune response to toxin (not as much of the whole dead again and less of a side effect profile)
Early on, the disease appears cold-like (catarrhal stage), but is very infectious. It is not just a pediatric illness, although they are most at risk, hence the effort for widespread vaccination, and with current CDC recommendations for Tdap coverage (tetanus toxoid, diphtheria toxoid, and acellular pertussis) during pregnancy and during adulthood.
Attachment to the airway cells is enhanced by filamentous hemagglutinin and pertussis toxin. The acellular pertussis vaccine is directed against those two agents.
Other toxins help to elevate cAMP and interfere with neutrophil function.
The tight adhesion of the bacterium accounts for the need of a swab from the posterior nasopharynx for culture.
Burkholderia species
- Pathogen category: G- rod, aerobic
- Source: environmental (soil and water) from SE Asia
- Virulence: toxin similar to Pseudomonas including pyocyanin
- Clinical: meliodosis with susceptibility with diabetes, chronic renal failure, ICP; glanders in horses
- Immune response: cell mediated; can relapse
- Treatment/Prevention: ceftaidime or carbapenems with shifting to oral sulfadrugs after initial IV meds
- Only takes a few to infect (bioterrorism)
As the older name of Pseudomonas pseudomallei suggests, Burkholderia is a Gram-negative environmental rod, particularly found in soil and water in Southeast Asia. Inhalation or inoculation can trigger meliodosis, but that can have chronic effects as well. It takes only a few bacteria to infect from an aerosol attack, hence the concern of bioterrorism (and why on the NYS notifiable condition list, as are many of the organisms that we cover; https://www.health.ny.gov/forms/instructions/doh-389_instructions.pdf). Doesn’t take a lot to trigger disease in inhalation, atypical pneumonia widespread infected pattern, abscess. Pneumonia plus and dialing up the ranks with more problems.
Chlamydia (Chlamydophila) pneumoniae
- Pathogen category: poorly G staining since no peptidoglycan, intracellular
- Source: human reservoirs spread by respiratory droplets
- Virulence: life cycle with elementary (extracellular that is the infectious phase phagocytosed by the next cell) and reticulate bodies (multiplies in cell’s phagosome)
- Clinical: atypical PNA or bronchitis; persistent cough; more in elderly
- Immune response: neutrophils help to clear; strong inflammatory response (like pelvic inflammatory disease with C trachomatis)
- Treatment/Prevention: tetracyclines or macrolides; immunity is not long lived
- Diagnosed by serology or nucleic acid probe assays
Features of interest for Chlamydia and the related genus of Chlamydophila (slightly different genome size and ribosomal features compared to Chlamydia; the organisms below have been recently reclassified as Chlamydia):
Elementary bodies spread aorund and spores to infect nearby cells turning into reticulate body generating rabid growth and multiplication before degeneration elementary body again (similar to virus). Have a cell wall lipopolysaccharide. Strong inflammatory response to kill off reticulate bodies and new batch of antibodies going around with many strains and not able to catch up to the strain with different stages immunologic memory wont be able to avoid the next infection. Gets in there and established can get patchy not a lot of cell wall to target doing ribosomal approach (tetracycline, ezithromycin, doxycucline)
small intracellular obligate parasites that are treated with tetracyclines or macrolides for several weeks, as they are slow growing and persistent.
Gram negative-like cell wall—no peptidoglycan but LPS (some)
life cycle of intracellular reticulate body that multiplies in the cell’s phagosome and the extracellular elementary body that is the infectious phase phagocytosed by the next cell
although they generate a strong inflammatory response that is cell-mediated (think of pelvic inflammatory disease scarring with C. trachomatis) with a number of innate responses, immunity to chlamydias is not long-lived, and so runs the risk of additional inflammation from repeated infections (Darville & Hilke, 2010, p. 116).
Chlamydia [Chlamydophila] pneumoniae: a common, but not severe, bronchitis or pneumonia, associated with persistent cough; tends to be more in the elderly compared to Mycoplasma. The organism is diagnosed by serology (problematic, because of the possibility of repeated infections) or nucleic acid probe assays.
Chlamydia (Chlamydophila) psittaci
- Pathogen category: poorly G staining since no peptidoglycans, intracellular
- Source: bird reservoirs
- Virulence: life cycle with elementary and reticulate bodies; spread through lymph nodes to generate a systemic response
- Clinical: atypical PNA, may disseminate into possible lethal infection
- Immune response: neutrophils help to clear
- Treatment/Prevention: tetracyclines or macrolides
- Diagnosed with serology
Chlamydia [Chlamydophila] psittaci: psittacosis (ornithosis) is an atypical pneumonia from exposure to infected birds or their droppings. The organism can spread through lymph nodes and so generate a systemic response in severe cases. As with C. pneumoniae, diagnosable through serology.
Corynebacterium diphtheria
- Pathogen category: G+ rod (pleomorphic shape- Chinese characters), aerobic, extracellular
- Source: human reservoir, spread by respiratory droplets
- Virulence factors: diphtheria toxin, blocks protein synthesis
- Clinical: diphtheria with oropharyngeal pseudomembrane; cardiac damage
- Immune response: antibodies to toxin
- Treatment/Prevention: DTap; antitoxin and penicillin or erythromycin for active infection
Corynebacterium diphtheriae should be rare, given the readily available inactivated toxin vaccine, but with respiratory droplet transmissibility, international travel, and decreased immunization rates, it needs to be recognized if present with its feature of pseudomembrane production. Diphtheriae is always around us and is a human based organism, that is found in breakdwon of ehalth systems.
Features of interest with C. diphtheriae:
Gram positive pleomorphic rod (“Chinese characters”), with antitoxin to decrease the toxin effect and macrolide or penicillin appropriate to decrease the bacterial number (Sanford Guide 2018)
The toxin inhibits cellular protein synthesis (by shutting down ribosomal elongation factor-2), which leads to epithelial cell death. This leads to the formation of a pseudomembrane as result from acute inflammation with fibrin, pus, and mucus. Toxin having a component- activation, b for binding. Shuts down ribosomal activity causing massive deliberate shutdown of humanicidal leading to dead white cells and fiber.
Myocarditis can also occur and be lethal, along with asphyxia from the pseudomembrane. Toxin can circulate into kidney, brain, or accumulate neough in myocarditis. Peniccilin as well as direct anti-toxin as passive immunization, TDAP, wanting them to form active antibodies and prevent ongoig spread and circulation of toxin to the heart.
Fusobacterium necrophorum
- Pathogen Category: G- rod, anaerobic, extracellular
- Source: normal flora of oropharynx
- Virulence factors: LSP and other G- features
- Clinical: pharyngitis, Lemierre syndrome
- Immune response: neutrophils
- Treatment/Prevention: for Lemierre syndrome- piperacillin + taxobactam; carbapenem; metronidazole + ceftriaxone; clindamycin (if PNC allergy)
- Lemierre syndrome- can generate infection extending to the posterior, lateral pharynx that can trigger internal vein thrombosis
While a normal flora component of the mouth, Fusobacterium necrophorum with a bacterial pharyngitis, often similar in presentation to strep throat. Where F. necrophorum is of concern is its association with Lemierre syndrome that can generate an infection extending to the posterior, lateral pharynx can trigger internal jugular vein thrombosis.
Causes bacterial meningitis- localized sepsis, enhancing thrombosis and if it isnt recognized can loalize thrombosis on cellultis pattern closer to IJV. Pennicillins even specizlied unable to interact and have to use cephalosporins.
Haemophilus influenza
- Pathogen category: G- rod, aerobic, extracellular
- Source: human reservoir with many strains as normal flora, spread by respiratory droplets
- Virulence factors: capsule, IgA protease, beta lactamase
- Clinical factors: meningitis, epiglottitis, OM (usually without capsid)
- Immune response: Igs to capsule, complement
- Treatment/Prevention: Hib vaccine; ceftriaxone
- Epiglottitis- medical emergency; risk of respiratory arrest; present with sore throat, drooling and difficulty swallowing and breathing
Other bacterial head and neck infections
Haemophilus influenzae: encapsulated strains are responsible for otitis media, sinusitis, epiglottitis, and meningitis, fortunately now rarer with the Hib vaccine.
Features of interest with H. flu:
Gram negative rod with capsule (b serotype most common and the one vaccinated against), so late-generation cephalosporin an appropriate antibiotic choice
IgA protease is another anti-immune strategy along with the capsule
Epiglottitis, mostly from H. influenzae, is a medical emergency, with risk of respiratory arrest. It should be rare in children vaccinated with the Hib vaccine, but unvaccinated individuals, e.g., adults, can still present with a sore throat, drooling, and difficulty in swallowing and breathing (“dysphagia, drooling, distress”). Can develop a nasty acellultiis, if the body cant catch up can become meningitis. More typically see in otitis media, the flu or other kind of compromise of respiratory epithelium and establishing downstream (cephalosporins). Tripoding respiratory distress and drooling are common.
* Otitis media- often types not targeted by the Hib vaccine; penicillin; Augmentin against beta-lactamase if no progress
Klebsiella pneumoniae
- Pathogen category: G- rod, aerobic, extracellular
- Source: part of colonic flora (opportunistic), nosocomial
- Virulence: capsule, beta lactamase
- Clinical: PNA with red currant jelly sputum (exotoxin and proteases account for tissue damage) and abscesses; nosocomial UTIs
- Immune response: Igs to capsule
- Treatment/Prevention: multiple drug resistances; carbapenems as needed
Klebsiella pneumoniae: an opportunistic infection, e.g., generating a pneumonia with abscesses (currant-jelly sputum). Features of interest for Klebsiella pneumoniae. Klebseilla abscess- hospital based or tough living (capsule) red currant ejlly. Harder to kill with beta lactamase with higher level later generation cephalosporin
Gram negative rod with capsule
Environmental, opportunistic organism—may colonize the oropharynx of weakened individuals
multiple drug resistances, so that it will need coverage from agents such as carbapenems, although the reports of carbapenem-resistant Enterobacteriaceae such as Klebsiella continue to increase
endotoxin and proteases account for tissue damage
Legionella pneumophila
- Pathogen category: G- rod (poorly staining), aerobic, intracellular
- Source: contaminated water supplies (no person to person spread; resistant to chlorine)
- Virulence: prevents fusion of phagosomes and lysosome and so proliferates within alveolar macrophages
- Clinical: legionnaire disease (PNA, fever, diarrhea)
- Immune response: cell mediated
- Treatment/Prevention: azithromycin or respiratory quinolone
- Diagnosed with antigen assay (urine), fluorescent antibodies, or use of serology
- Culture n charcoal yeast extract agar
- CXR will show infiltrative processes
Legionella pneumophila: intracellular, Legionnaire’s disease with pneumonia, fever, and sometimes diarrhea, from contaminated air conditioning systems (no person-to-person spread), initially colonizing amebae (i.e., able to survive within phagocytic cells).
Older men dying of pneumonia that wasn’t a stypical pattern, gram negative, special charcoal medium for it to grow. Environemtnally hardy organism living inside organisms like amoebas in water persist inside phagocytic cell. Environment or organism not necessarily killed by chlorination and making biofilm with aerolisnzation from building wide AC building. Bacteria have ability to persist in pons can get aerosinolized and down to macrophages. Older people with lung disease have issues with macrophages not able to kill them because arent activated.
Once inhaled, Legionella will survive intracellularly in the macrophages by inhibiting phagosome/lysosome fusion, and subsequently release as a transmissive form (you can see why I am doing this after the chlamydiae).
This infection can trigger the macrophage to generate an inflammatory response that harms lung tissue.
Features of interest for L. pneumophila:
poorly-staining Gram negative rod, with respiratory fluoroquinolone (macrolide as alternative) recommended (Sanford Guide 2018)
aquatic environmental organism, resistant to chlorine
affects weakened individuals, e.g., elderly, as they mount less of a Th1 response to stimulate macrophages
Identification is done with an antigen assay (particularly done on urine), fluorescent antibodies (less popular), or use of serology, as Gram staining is difficult, as seen in the image.
In addition, in terms of culture, a specialized charcoal yeast extract agar is used, as Legionella is fastidious (difficult to grow out), taking several days.
As with other atypical pneumonias, the CXR of a patient with Legionella will show an infiltrative process.
Moraxella catarrhalis
- Pathogen category: G- diplococcus, aerobic, extracellular
- Source: human reservoir, upper respiratory tract
- Virulence: capsule, betalactamase (highest level)
- Clinical: OM in children, PNA in patients with COPD
- Immune response: antibodies to capsule
- Treatment/Prevention: amoxicillin with clavulanic acid
- Otitis media; penicillin; Augmentin against beta-lactamase if no progress
Moraxella [Branhamella] catarrhalis: is a Gram negative coccobacillus that is not as kidney-bean shaped as Neisseria. M. catarrhalis is a cause of pneumonia, particularly in those with previous lung disorders, as well as sinusitis or otitis media (the third major head and neck organism after pneumococcus and H. influenzae). M. catarrhalis shows high levels of beta lactamase production; can be covered by a variety of agents, e.g., later generation cephalosporin, Augmentin®, sulfa drugs, macrolides (Sanford Guide 2018). Look gonnorhea able to hang out and adhesants, not flushed away, not commonly capsuled. Likes to produce beta lactamases- periplasmic region cranks out self produced items cutting down on ability of cephalosporins to not get out. Start at amoxycillin and then augmentin.
Apircal scarring- hyperpenetration Tb secondary moraxella where tb started
Mycobacterium tuberculosis
- Pathogen category: acid fast bacterium, obligate aerobe, intracellular
- Source: human reservoirs, spread by respiratory droplet
- Virulence: lipid-rich cell wall
- Clinical: tuberculosis
- Immune response: delayed type hypersensitivity with caseating granuloma formation
- Treatment/Prevention: multidrug therapy involving isoniazid and others; BCG vaccine
- Ghon complex- primary infection fibrosis, usually hilar lung nodes
- PPD- type IV hypersensitivity with activated T cells (Th1)
- Military TB- secondary spread results from hemotogenous spread of the organism
Tuberculosis should certainly be a consideration for lung infections, particularly for those patients from high prevalence regions. Develops caseating granuloma. Primary foci ghon complex battle got sufficiently fought in the lymph node fibrosiing it. Milliary tb hematenous spread before fight begins. Targetting the fatty acids (mycolic acids) on the tb acid-fast coat.
TB and other mycobacteria are obligate aerobes, so it is not surprising that there is a predilection for the apices of the lungs with their high V/Q ratios.
Primary disease: wall off, fibrosis of Ghon complex of the original lung site and local hilar lung nodes
The PPD (purified protein derivative), as a 0.1 ml localized subcutaneous injection that represents a type IV hypersensitivity with activated T cells if there are Th1 cells that respond to the TB presence.
Secondary spread can occur if there is subsequent immunosuppresion. Miliary TB results from hematogenous spread of the organism.
As briefly suggested under the antimicrobial section earlier, a combination of medications, involving isoniazid and others depending on severity, e.g., rifampin, pyrazinamide, and ethambutol, will be needed for months in order to combat the mycobacterium.
Mycoplasma pneumoniae
- Pathogen category: no cell wall, aerobic, extracellular, slow growing
- Source: human reservoirs
- Virulence: adhesions (trigger ciliostasis) to respiratory cilia and no cell walls to target
- Clinical: atypical PNA (nonproductive cough for a week or more)
- Immune response: cleared by macrophages in mucosa
- Treatment/Prevention: macrolides
- Less alveolar exudate and more interstitial presentation on CXR
In contrast to the pneumococcus, the atypical pneumonias are subacute in onset, with a week or more of symptoms, e.g., nonproductive cough, before a patient will seek treatment. There is less alveolar exudate and a more interstitial presentation on chest film. No cell wall tiny bacteria can get into the lung and give off ciliary stasis to get in down toward respiratory bronchiole and conducting bronchiole and ciliary stasis and mucus movement out (patchy not fully lobar and localized) no cell wall so you canttarget that (doxy-ribosome)
The CXR for the common atypical pneumonia of Mycoplasma pneumoniae is more infiltrative than the lobar picture of pneumococcal pneumonia.
Mycoplasma pneumoniae: mycoplasmas have no cell walls, and so are not seen on Gram stain. With no peptidoglycan, macrolide coverage is useful.
Mycoplasma makes adhesion proteins that triggers ciliostasis, and hence access to the lower portions of the respiratory system.
Very small and slow-growing , so that therefore usually clinical diagnosis, and assays that follow antigens, e.g., cold hemagglutinins (antibodies that cross-react with RBCs) instead of Gram stain or other visualization techniques.
Pseudomonas aeruginosa
- Pathogen category: G- rod, obligate anaerobe, extracellular
- Source: multiple environmental exposures, nosocomial
- Virulence: glycocalyx, exotoxin A (diphtheria like), proteolytic enzymes, pyocyanin (blue pigment that damages host cells via reactive oxygen species), betalactamase
- Clinical: folliculitis, pneumonia, burns, OE
- Immune response: intact epithelia, functioning Igs, complement, neutrophils
- Treatment/Prevention: antipseduomal medications (piperacillin-tazobactam and tobramycin)
- Can be deadly for CF patients; if it causes PNA the proteases can lead to a hemorrhagic picture
- Otitis externa- typically a fuoroquinolone if moderate to severe
Pseudomonas aeruginosa is a pathogen that will show up in a number of contexts, given its minimal environmental requirements and large set of virulence factors. It can be especially deadly for patients with cystic fibrosis, and if it causes pneumonia, the extensive proteases can lead to a hemorrhagic picture.
Environmentally hardy- doesn’t need a lot of nutrients, otitis externa. Produces many toxins especially those who are immune compromised high in patients with cystic fibrosis and proteases smelling like grape (acetone). Pseudomonas- can become pneumonia RBC destroyed alveoli. Beta lactamases and drug resistance producing special anti-pseudomonal drugs to kill it cephalosporins and higher level penicillins.
Streptococcus mutans (viridans strep)
- Pathogen catergory: G+ coccus, aerobic, extracellular, chains
- Source: normal flora or oropharynx
- Virulence factors: glycocalyx; glucans to adhere to enamel; acids as result of sugar fermentation
- Clinical: caries, endocarditis
- Immune response: salivary defense proteins (lysosomes mainly, IgA and IgG in saliva)
- Treatment/Prevention: dental hygiene; dental procedure prophylaxis with amoxicillin
- Can also result in trismus, inability to open mouth with peritonsillar abscess
- Ludwig angina- rapid spreading bilateral infection in the submandibular space that imitates with dental abscess
Streptococcus mutans (viridans strep): oral flora; implicated in dental caries. A film (pellicle) derived from salivary proteins allows the initial attachment of these oral streptococci, with other organisms adding on. The acids from bacterial metabolism damages the mineralized enamel. Anaerobic organism have (streptococcus mutans- lesser hemolytic bacteria) biofilms that is placed on enamel with glycosugar and can get actinomyces and fusibacteria and while metabolziing sugar biofilm the bacteria release acid destroying your enamel. With plague, dry sticky adhering biofilm that is cleaned off to prevent more.
A review of head and neck anatomy can help to account for different presentations of infections in the region, e.g., trismus or the inability to open the mouth with a peritonsillar abscess.
Polymicrobial disease can get among fascial plane and cellulitis making it a tight peritonsillar fit developing ludwig angina.
Ludwig angina is a rapidly spreading bilateral infection in the submandibular space that typically initiates with a dental abscess, with a polymicrobial infection of Streptococcus mutans and others.
Streptococcus pneumoniae
- Pathogen category: G+ coccus, aerobic, extracellular, lancet shaped diplococci
- Source: normal flora of upper respiratory tract
- Virulence: capsule (prevent PMN binding and phagocytosis), IgA protease (disease stays in anatomical boundaries-lobar), adhesins
- Clinical: lobar pneumonia (rigor triggered by IL-1; rusty sputum from capillary leakage), meningitis, sinusitis, OM
- Immune response: Ig formation to capsule, complement, neutrophils
- Treatment/Prevention: penicillin; sensitive to other respiratory agents depending on local resistance; vaccine targeting capsule antigens
- Detected by latex agglutination from CSF
- Otitis meda; penicillin; Augmentin against beta-lactamase if no progress
Pathogenic strains of the pneumococcus have a thick capsule to prevent PMN binding and phagocytosis (although it can still get opsonized, as with the pneumococcal vaccine). S. pneumoniae does not produce a lot of proteases, so that the disease stays within anatomical boundaries (hence the picture of lobar pneumonia on CXR). A single rigor (triggered by cytokines like IL-1) follows an abrupt onset. The rusty sputum results from capillary leakage following the lung invasion (see how many WBCs are in the alveoli). Pleuritic chest pain can follow peripheral lung involvement. Classic pneumar pneumonia, most exist with the capsule doing complement activating and hiding makign it more infections. Chills- reset of thermostat, rust colored sputum from leakage of neutrophils into the alveolar space making it leaky and rust-colored sputum. Penicillin should work with pneumococcal strains higher up the ration of drugs. Pneumococal vaccine so you have the capsule and able to phagocytoze before this point.
Pneumoccocus- alevoli filled with neutrophils generating enough inflammation to get leakage into the alveolus and filling it with neutrophils and consolidation. Macrophages- activated enough by presence of pneumococcus phagocytossize the aftermath to fairly normal anatomy.
Additional features of interest for S. pneumoniae:
Gram positive lancet-shaped diplococcus, alpha hemolytic
may be part of normal flora, spread by respiratory droplets
may be detected by latex agglutination test in CSF, as it is a common agent for meningitis
treatment for pneumococcal pneumonia focuses on penicillin or respiratory quinolones, although macrolides or doxycycline may also cover strains.
The pneumococcus can be normal oropharyngeal flora in much of the population, so be sure that the sputum sample is of good quality to characterize it as the presumptive agent for a patient’s pneumonia, looking for the lancet-shaped diplococcus following Gram stain.
Streptococcus pyogenes (group A strep)
- Pathogen category: G+ coccus, aerobic, extracellular
- Source: normal flora of oropharynx and skin, disease with penetration
- Virulence factors: streptolysin O (beta hemolysis), erythrogenic toxin, M protein blocks complement, capsule, hyaluronidase, streptokinase, peptidase (destroy C5a)
- Clinical: impetigo, cellulitis, necrotizing fasciitis, pharyngitis, scarlet fever
- Immune response: Ig formation to M protein neutrophils, cross-reactive antibodies can generate rheumatic fever
- Treatment/prevention: penicillin
- Adhesins- lipoteichoic acid and protein F
- M protein- complement opsonization, anticomplement like human cells, can lead to autoimmunity, used to evade immune system
- Erythrogenic exotoxin (superantigen) accounts for scarlet fever; multiple papules creating sandpaper textured skin
Group A streptococci can cause a number of illnesses, thanks to adhesins usch as lipoteichoic acid and protein F that bind to fibronectin, and a variety of other virulence factors that include proteases, DNases, streptokinase, streptolysins, and an antiphagocytic capsule. M protein is a streptococcal feature that interferes with complement opsonization (binds fibrinogen and complement protection proteins) that is highly variable among strains at the A region; cross-reactive antibodies to certain pharyngeal strains may contribute to rheumatic fever. Antibodies against it might cross-react with normal tissue leading to rheumatic fever.
Adhesive pili- sticks to cells. Techoic acids stabilize things along the way.
F protein- fibronectin common component of the extracellular matrix and mimic normal features to successfully adhere to the surface of the celll. Techoic acids- hold onto and stabilize wall, have other carbs and also anchro the cell wall and membrane. Pennicilin and beta lactam may not work because of resistance but is the first line and thing you try.
Streptococcus is a Gram-positive coccus that grows in chains, and is beta-hemolytic (hemolysin and breaking open red cells and then eating hemoglobin), as shown by the hemolysis on a blood agar plate.
Trigger toxins and destroy RBCs
Streptococcus pyogenes (Group A strep)
Pathogen category: G+ coccus, aerobic, extracellular, in chains
Source: normal flora of oropharynx and skin, disease with penetration
Virulence factors: streptolysin O (beta hemolysis), erythrogenic toxin, M protein blocks complement, capsule, hyaluronidase, streptokinase, peptidase (to destroy C5a)
Clinical: impetigo, cellulitis, necrotizing fasciitis, pharyngitis, scarlet fever
Immune response: Ig formation to M protein, neutrophils. Cross-reactive antibodies can generate rheumatic fever.
Treatment and/or prevention: penicillin
