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80 Cards in this Set
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Dx rheumatic fever?
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strep-pyogenes
ASO titer - streptolysin O is oxygen-labile hemolysin that is neutralized by cholesterol in skin; ASO titer is less useful in skin infections because Streptolysin O is bound to cholesterol here --> not available for antigen presentation |
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streptokinase use?
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Strep C produce this and it activates plasminogen to disrupt blood clots
for coronary artery occlusion -careful w/ hypersensitivity if Pt was previously exposed |
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anti-DNAse B titer?
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Dx for strep even in skin infection because DNAse is not bound by cholesterol in the skin
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pharyngitis/tonsillitis (strep) clinical
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abrupt onset of sore throat with malaise , fever, headache (nausea, vomiting and abdominal pain is common in children)
examination shows edema & lymphoid hyperplasia of posterior pharynx, red tonsils, exudates, tender enlarged mandibular lymph nodes & T > 101F |
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Pyroderma
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Impetigo: superficial skin infection with papule-vesicle-pustule-crust stages due to S.pyogenes +/ S. aureus
leads to towel household spread |
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scarlet fever
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strawberry tongue, sandpaper rash,
from pharyngitis, S.pyogenes that makes erythrogenic toxin as consequence of being infected by a PHAGE |
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cellulitis/lymphangitis
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mostly S.pyogenes
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erysipelas
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form of cellulitis with diffuse lymphangitis of skin--> spread via lymphatics with redness & pain at te advancing margins
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streptococcal cellulitis / erysipelas with risk?
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venous & lymphatic compromise Following axillary lymph node dissection for breast carcinoma
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STSS
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streptococcal toxic shock syndrome:
Hypotension: BP <90mmHg AND >2 of these: -renal impairment -coagulopathy -liver involvement -acute respiratory distress syndrome -generalized erythematous macular rash that may desquamate -soft tissue necrosis (necrotizing fasciitis, myositis or gangrene) |
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jones criteria tell you what?
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rheumatic fever dx
2 major OR 1 major + 2 minor |
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major and minor Jones
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Major:
carditis, polyarthritis, chorea, erythema marginatum, subcutaneous nodules |
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erythema marginatum
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one of the major classifications of the Jones criteria for rheumatic fever
early in clinical manifestation detected in 10% of children & fewer adults painless, eythematous, nonpuitis, blanching dermatitis, |
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glomerulonephritis after strep infection
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Post-Streptococcal Glomerulonephritis
Occurs following skin OR pharyngeal infections; Due to deposition of immune complexes in the glomeruli of kidneys; Manifestations include: edema of face & extremities; hematuria; hypertension; less complement levels; abnormal urinary sediment. Chronic renal disease can result. |
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guttate psoriasis
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acute guttate psoriasis typically 1-2wks after infection with gr A strep
pt have increased Vb2 = T cells in theri skin lesion streptoccal pyrogenic exotoxin C is thought to be involved |
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what leads from GBS infected mother to early-onset GBS infection in neonate?
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strain virulance --> more genital inoculum --> premature rupture of membranes --> preterm delivery --> prolonged rupture of membranes --> decreased serum concentration fo serotype specific IgG
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Strep agalactiae
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most in peripartum period and in the newborns either late or early
early-onset: within 5 days and usually present in 1-3 manners: Bacteremia without an indentifyable focus pneumonia meningitis late onset: 7days to 3 months --> bacteremia with meningitis is a common presentation |
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streptococcus gallolyticus
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bovis
group D bacteremia, endocarditis due to S.gallolyticus have associations with lesions from mouth to anus but adenocarcinoma is the strongest MIC 1yg.ml, very sensititve to penicillin! must do colonoscopy |
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enterococcus
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faecalis (80-90%)
facium (5-10%) are most important relatively resistant to penicillin compared to the other group D strep! causes: endocardidits, UTI intraabdominal and pelvic and wound spntaneous peritonitis nosocomial bacteremia RARE CNS infections |
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resistance of enterococci
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high lvl of aminoglycoside resistance:
-plasmid aquisition of AG modifying enzymes (gentamycin MIC > 500ym/ml) alterations of peniclillin-binding proteins -- beta-lactamase resistance also beta-lactamase production (penicillin and ampicillin resistant) vancomycin resistance from the altered D-alanyl-D -alanine on the peptidoglycan side chain! |
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viridans strep
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S. mitis,
S. sanguis S. salivarius S. mutans alpah hemolytic but not afraid of the chin- resistant to optocin (not like S. pneumonia susceptible) caries -especially S. mutans |
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milleri group
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S. anginosus
S.morbillorum S.constellatus S. intermedius -nl in bowel and cause direct hematogenous spread to normally sterile areas |
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anaerobic strep
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peptostreptococcus, peptococcus,
nl in the GI and female GU cause problems when they end up in nl sterile locations bc altered anatomy, poorly perfused tissues or trauma and as usually associated with other organisms |
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most common anaerobic strep for diabetic foot ulcer?
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peptococcus
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special features about the streptococcal structure
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protein A
coagulase collagen binding protein elastin-binding protein fibronectin binding protein clumping factor enterotoxin B TSST-1 alpha-toxin peptidoglycan: -shape, stability, 50% of weight, carbohydrates cross-linkes, pasic ptoerties: elicit TNF-production, PMN toxicity, Endotoxin-like activity, complement activation, elicit opsonic antibodies teichoic acid is in the cell wall of gram + --> it is 40% of the cell wall and it's covelently bound to peptidoglycan lipoteichoic acids bound to lipid membrane adherence ligands to mucosal receptor sites (instead of pili I guesS) when bound to peptidoglycan they elicit specific antibody formation |
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capsule
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microcapsule: just external to the cell wall -> serotyping, 80% of Dx cause by sertypes 5&8, immogenicc, Ab facilitates opsoniphagocytes
-capsule presenton only a few strains and not clinicallt important slime is loosely adherent and maybe important in pathogenesis |
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protein A use
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streptococci have thse proteins incorpoated in to their membares
they are binding to Fc receptors of al human immunoglobulin G subclasses except IgG2 - antiphagocytic |
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staphylococcal enzymes
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catalase, hyaluronidase, some have coagulase (aureus)
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community aqured MRSA have this toxin
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panton-valentine leukocidin
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TSST-1 protection
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to protect from the cytokine storm that these superantigens create, we can make antigens. however 80% fail to make these antibodies
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exfoliatins
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responsible for scalded skinsyndrome
act on cells at the lvl of the statum granulosum to produce rash, blisters & exfoliation act as superantigens antibody is protective |
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atopic dermatitis and eczema can predispose to
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S. aureus colonisation
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what do the products of S. aureus do?
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they stimulate the PMN chemotaxis to the infected site --> opsonization od S. aureusmust first actvate the complement system --> Ig to peptidoglycan, teichoic acid or microcapdusle in the immune subjects, protein A impairs phagocytosis (binds the Fc receptors!!)
deficiencies of Ig or complement impairs opsonization |
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compare the # of staph needed to cause infection in the intact skin
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> 10 000 000 S. aureus in intact skin compared to 100 on the suture
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another name for carbuncles
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boils. deep seated infections around the hair follicle resut from coalesclece of furuncels
treat with hot compresses, I and D as necessary and appropriate |
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fomite
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A fomite is any inanimate object or substance capable of carrying infectious organisms (such as germs or parasites) and hence transferring them from one individual to another. A fomite can be anything (such as a cloth or mop head), so when cleaning, it is important to remember that such items could aid the spread of pathogenic organisms. Skin cells, hair, clothing, and bedding are common hospital sources of contamination.
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hidradenitis suppurativa
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disfiguring infection of apocrine sweat glands that involve groin, perineum
most often in african american tx: antistreptococcal antibiotics and surgical debrisment |
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most common staphyloccoal soft tissue infection
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pus collections that must be drained
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most common causes of otitis media
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what a bunch of Shmoc in your ear!
Streptococcus pneumoniae Moraxella catarrhalis Haemophilus influenzae |
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what are some bad results of S. aureus?
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Bacteremia & Endocarditis
primary bacteremia without an obvious focus of infection (e.g. parenteral drug addicts) --> endocarditis also in this category -secondary to another site of infection (e.g, skin abscess, IV catheter, pneumonia.. ) |
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how do you manage S. aureus bacteremia?
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I and D the 1 focus, if one is present
bc of prevalence o MRSA, culture and susceptibility testin are ssential doe appropriate x assume first that it's methicillin resistant and then then adjust the therapy once resulre of suscpetibility are available - vancomycin is an inferior agent if organism tunrs out to be meth suscptiple If complicated, treat 4-6 weeks; if not, 10 days; Know vanc is inferior to B-lactam!!! |
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osteomyelitis
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S. aureus is most common cause of osteomyelitis
3 pathophysiiologic results in osteomyelitis: -bacteremic spread to long bones of children and vertebrae of adults -contguous to another site of infection -vascular insufficiency tx with surgical debridement & prolonged antibiotic therapy |
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most common cause of pyomyositis?
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infection within a muscle - S. aureus
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staphylococcal scalded skin syndrome
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S. exfoliatin
<5yo children local S. aureus infection in the nasopharynx, umbilicus or UT Rx: antibiotics and supporive skin care |
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CDC surveillance case definition for the staphylociccal toxic shock syndrome
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hypotension: systolic <90
fever: >38.9C rash: diffuse macular erythroderma desquamation: 1-2wk after onset of illness, particularly of palms& soles and : Multisystem involvement: 3 of the following: GI: vomiting or diarrhea; Muscular: severe myalgia or CPK; Mucous membrane – vaginal, oropharyngeal or conjunctival hyperemia; Renal: BUN &/or creatinine > 2X ULN; Hepatic: Total bilirubin, AST or ALT > 2X ULN; Hematologic: platelets 100,000; CNS: disorientation or alterations in consciousness. Negative results for Rocky Mountain spotted fever, leptospirosis, or rubeola; Negative blood, throat or CSF cultures (except for S. aureus). |
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infections from coagulase - staph
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UTI - hospital aquired - usually S. epidermidis in association with Ucath
outpatient - S. saprophyticus is 2nd most common caus of UTI in young women bacteremia in critically ill or immunosuppressed patients, related to vascular catheters native valve endocarditis - unusual & occurs in - patients with abnormal cardiac valves -parenteral drug addicts |
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Tricuspid Valve Endocarditis due to ______________ with Septic Pulmonary Emboli
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Tricuspid Valve Endocarditis due to Staphylococci cohnii with Septic Pulmonary Emboli
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who is responsible for 30% of the post op sterneal infections?
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coagulase - staphylococci
rarely causes hematogenous osteomyelitis in bones underlying ischemic or pressure ulcers |
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inducible resistance?
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extracellular enxymes that disrupt the b-lactam ring of penicillins & result in penicillin resistance: inducible and coded on plasmids - 99% expression
order of susceptibility to b-lactamsees: penicillin >>>>> dicloxacillin > cloxacillin > oxacili > nafcillin clinically significant; only 5% of S. aureus are now susceptible to penicillin |
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HA-MRSA
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risks: hemodyalisis, CAPD IV drug abuse, dermatitis, IDDM, burns, antibiotics, long hospitalization, greater severity of underlying illness
-organisms tend to be resistant to multiple classes of antibiotic, not just b-lactams |
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CA MRSA
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Genetically, CA-MRSA are different than HA-MRSA, and carry the small, unique SCCmec Type IV mobile genetic elements.
This suggests that these organisms did not originate from hospital strains that disseminated into the community. The majority of infections are skin & soft tissue (frequently complicated), but patients have developed invasive pneumonias, bacteremias, endocarditis & osteomyelitis. >60% of staphylococcal isolates from the community are CA-MRSA in many Houston hospitals (TCH, MEDVAMC, Ben Taub, etc.) |
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MRSA strains that demonstrate discordance between erythromycin susceptibility & clindamycin susceptibility (ClinS/EryR) may have 2 responsible mechanisms that have clinical significance:
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msrA encodes an ATP-dependent efflux pump that confers resistance only to 14- & 15-membered ring macrolides & type B streptogramins, but not to lincosamides (e.g., clindamycin, which will be sensitive).
iMLS inducible macrolide-lincosamide-streptogramin B resistance due to presence of erythromycin ribosomal methylase (erm) genes. Clindamycin therapy induces resistance. detect with double-disk diffusion assay (D test). |
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VISA Strains of MRSA
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9 reported cases of VISA in Japan (5 patients) and USA (4 patients: MI, FL, NJ, TX);
Most patients had indwelling catheters (frequently, a dialysis catheter); All patients had received prolonged vancomycin therapy, usually inappropriately; MIC90 for vancomycin = 8 g/ml; Mechanism of resistance not well delineated thicker cell wall? Remain susceptible to other antibiotics (TMP/SMX, minocycline, rifampin). Patients appear to respond to vancomycin + -lactamase combinations how did we get VISA? It has recently been shown that S. aureus produces a sex pheromone that can stimulate an enterococcal vancomycin-resistant conjugative plasmid. It is highly likely this occurred in patients’ wounds that were colonized with both VRE & MRSA. |
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Corynebacterium diphtheriae
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Morphology and Properties Club shaped, gram (+) bacilli; metachromatic granules; fastidious; reduces tellurite; non-hemolytic
Disease Respiratory and cutaneous Pathogenesis/Virulence Diphtheria toxin ADP-ribosylates EF2 Epidemiology Spread by droplets or direct contact with skin abrasions Diagnosis Gram-stain; Elek immunodiffusion or PCR for toxigenicity Treatment Antibiotics, antitoxin (DAT) and vaccination Morphology and Properties Club shaped, gram (+) bacilli; metachromatic granules; fastidious; reduces tellurite; non-hemolytic Disease Respiratory and cutaneous Pathogenesis/Virulence Diphtheria toxin ADP-ribosylates EF2 Epidemiology Spread by droplets or direct contact with skin abrasions Diagnosis Gram-stain; Elek immunodiffusion or PCR for toxigenicity Treatment Antibiotics, antitoxin (DAT) and vaccination Diphtheria toxin is encoded by a beta-phage and its expression is repressed in the presence of iron Respiratory Transmission: Droplets Symptoms: Sore throat, fever (<102°F), enlarged lymph nodes and edema in neck, malaise Pathology: Pseudomembrane of neutrophils, fibrin, and epithelial cells that covers the throat Systemic effects: Myocardial damage, arrhythmia, myocarditis, and congestive heart failure Cranial and peripheral neuropathy and paralysis 2. Cutaneous Transmission: Direct contact with infected abrasions Symptoms: Impetigo-like lesions on arms or legs Pathology: Localized ulcers Systemic effects: Rare |
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Listeria monocytogenes
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Morphology and Properties Gram (+), motile, club-shaped bacillus; weakly hemolytic; tellurite resistant; multiplies at 4°C
Disease Maternal listeriosis; sepsis, meningitis, focal infections in immunocompromised Epidemiology Contaminated food and water; transmission to fetus Pathogenesis/Virulence Invades intestinal MØ (internalin), escapes vacuole (listeriolysin O), then moves from cell to cell via actin filaments (ActA) Diagnosis Diphtheroid in blood or spinal fluid; motile at 22°C vs. 37°C; cold enrichment for growth of the organism; genetic fingerprinting Treatment Antibiotic therapy (ampicillin + gentamicin); must penetrate host cells |
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anthrax toxins
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LF= MAPKK endopeptidase induces cytokine production
and leads to cell deregulation and shock EF = Cam-dependent adenylate cyclase cause edema and deregulates leukocytes Morphology and Properties Gram (+), sporulating, nonmotile encapsulated bacillus Disease Pulmonary, cutaneous, gastrointestinal Epidemiology Aerosols, skin contact and contaminated meat Pathogenesis/Virulence Tripartite toxin, polypeptide capsule Diagnosis Gram (+) rods in chains; susceptible to penicillin |
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Bacillus anthracis
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Cutaneous (95% of cases)
Occurs mainly on arms, neck and face Initiates as a small papule then progresses to a necrotic eschar surrounded by inflammation Swelling (edema) is common Lesion is painless Intestinal Acquired by ingestion of spores in grossly contaminated meat Nausea, vomiting and diarrhea result from gastrointestinal invasion Pulmonary (Woolsorter’s Disease) Acquired by inhalation of spores (hides or raw wool) Initial influenza-like symptoms progress to severe respiratory distress (not a true pneumonia) Usually fatal within 1 to 2 days of onset of acute symptoms 1. Transmission Primarily a disease of sheep, cattle and horses, but human contact with infected animals or animal products and aerosols (hair, bristles, hide, wool, bone, etc.) can cause transmission. Three means of inoculation (no person-to-person transmission); Cutaneous: Inoculation via breaks in the skin: papule ulcerates to a black eschar (es’kar) with edema (80% resolve, 20% progress) Intestinal anthrax (near 100% mortality): Occurs 2-5 days following ingestion => abdominal pain, bloody diarrhea, vomiting Pulmonary (not a true pneumonia): Biphasic disease beginning with flu-like symptoms (3-10 days) that progresses to acute phase characterized by pulmonary edema, hemorrhagic pneumonitis, and septicemia (100% mortality) 2. Disease Spores are phagocytosed by macrophages then germinate Vegetative bacteria released into lymphatic system, multiply, then are released to bloodstream Death is due to septicemia, toxemia and shock |
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Bacillus cereus disease
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Food poisoning (toxin mediated)
Emetic Rapid onset (1-6 hrs) with vomiting characteristic Commonly associated with ingestion of stir-fried rice Heat stable small cyclic peptide toxin (cereulide) Gastrointestinal Delayed onset (8-16 hrs) with abdominal cramping and diarrhea Associated with meats and vegetables Protein toxin activates fluid influx into intestine Invasive disease Eye infection: associated with metal injury to the eye Cellulitis: in the immunocompromised 3. Pneumonia Rare, but observed, in the immunocompromised 4. Cutaneous infection Newly identified Transmission is by ingestion of vegetative bacteria that germinate from spores. Need >106 bacteria per gram of food to get disease. Two Enterotoxins, Two Diseases Emetic (cereulide): rapid onset (1-6 hr) vomiting, fried rice-CATERERS. Mimics staph. Pre-formed emetic toxin is heat stable Gastrointestinal: delayed onset (8-24 hrs), with diarrhea, meat, veg. Gastrointestinal toxin produced by germinating spores is heat labile Gastrointestinal disease is self-limiting 2. Invasive disease Soft tissue disease (cellulitis) can occur in leukemics or other immunocompromised Eye Infection: direct trauma to the eye, heroin addiction (hematogenous spread). 3. Pulmonary Infection: compromised patients. Morphology and Properties Gram (+), sporulating, motile bacillus; no capsule Disease Food poisoning; eye infection; pulmonary infection Epidemiology Ingestion of bacteria; intraocular inoculation; opportunistic infection in immunocompromised Pathogenesis/Virulence 2 Enterotoxins (gastrointestinal and emetic); lecithinase; hemolysin Diagnosis Motile, gram (+) rods in chains; hemolytic; resistant to penicillin Treatment Antibiotic therapy (resistant to ß-lactams); not necessary in emetic or gastrointestinal disease |
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differential vs selective media
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ifferential media or indicator media distinguish one microorganism type from another growing on the same media.[5] This type of media uses the biochemical characteristics of a microorganism growing in the presence of specific nutrients or indicators (such as neutral red, phenol red, eosin y, or methylene blue) added to the medium to visibly indicate the defining characteristics of a microorganism. This type of media is used for the detection of microorganisms and by molecular biologists to detect recombinant strains of bacteria.
Examples of differential media include: * Eosin methylene blue (EMB), which is differential for lactose and sucrose fermentation * MacConkey (MCK), which is differential for lactose fermentation * Mannitol Salt Agar (MSA), which is differential for mannitol fermentation * X-gal plates, which are differential for lac operon mutants Selective: allow enteric gram negative rods to grow while suppressing growth of other organisms Lactose negative: Salmonella, Shigella, Proteus, Yersinia |
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fcts of capsule
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defense - shielding from complement, and camouflage resempling host
-resistance to drying biofilm formation Bacterial pathogens often have polysaccharide capsules which allow them to resist engulfment by phagocytes. Complement (nonspecific) and antibody (specific) must bind to the capsule to opsonize the bacteria and permit uptake by phagocytes. Classical complement pathway is Ag/Ab complexes—results in C3 activation, binding to bacterial surface, and opsonization. C3 activation is largely confined to the surface upon which it is initiated—thus held away from the organism by capsule. E. coli K1 capsule resembles a host antigen. |
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where can we find the virulent E. coli?
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more likely in the urine -
E. coli causing UTI have certain virulence genes not found as often in stool isolates Type-1 pili enable bacteria to colonize the bladder: recognize mannose-containing receptors on host cells P-pili enable bacteria to colonize ureters and kidney: recognize P antigen receptors (alpha-gal-1> 4 beta gal) Virulence factors not essential for infection of compromised host Example: catheter-associated UTI |
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who gets infected w/ klebsiella?
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Pathogen in healthy people
UTI, pneumonia Causative agent of multiple nosocomial infections: Pneumonia, UTI, biliary infection, peritonitis, wound infection Mucoid capsule Resistant to ampicillin Chromosomally-encoded β-lactamase “Currant-jelly” sputum associated with Klebsiella pneumoniae pneumonia. Seen in compromised hosts: alcoholics, COPD, intubated. Friedlander’s disease: propensity for upper lobes, abscess formation, hemoptysis, severe, bulging fissure sign on CXR caused by edematous lobar consolidation—yet often hard to distinguish clinically from other bacterial pneumonias |
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Proteus mirabilis
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Associated with long-term use of urinary catheters
Produces urease, which causes crystal formation Highly motile Proteus was the son of a sea god who could change his shape |
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Enterobacter
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Lactose fermenters, mucoid
Source: Most common: endogenous intestinal flora Patient-to-patient spread Common source outbreaks Opportunistic pathogen Intrinsically resistant to ampicillin Chromosomal β-lactamase Inducible High baseline mutation rate |
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Serratia marcescens
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Widespread in environment
Truly an opportunistic pathogen Was thought to be so harmless that used by Navy in studies of airborne distribution of organisms Causes nosocomial infections Infections in IV drug users Endocarditis, osteomyelitis |
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Citrobacter
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Catheter-associated UTI
C. diversus: brain abscess in neonates |
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Pathogenesis by ETEC strains
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Fimbriae adhere to intestinal mucosa
Elaborate one or both of two enterotoxins Heat stable (ST) increases cGMP Heat labile (LT) increases cAMP Very similar to cholera toxin AB toxin Both act on the CFTR to cause secretion of chloride into the lumen Enterotoxin = an exotoxin that acts upon GI epithelium to increase fluid secretion Mechanism of action of Escherichia coli heat-stable (ST) enterotoxin on guanylate cyclase |
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ETEC: Prevention and Treatment
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Prevention: boil it, bake it, peel it
Bismuth subsalicylate: prophylaxis and treatment Antibiotics are effective but not necessary Fluoroquinolones |
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ETEC
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ETEC
Most common cause of travelers’ diarrhea No fecal leukocytosis No fever |
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Enterohemorrhagic E. coli (EHEC) Shiga Toxin-producing E. coli (STEC)
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Cause of outbreaks of bloody diarrhea
Bagged spinach, Taco Bell, hamburger meat Shiga toxin kills the host cell Destroys ribosomal protein synthesis Reservoir: GI tract of cattle and large herbivores Organisms survive in the environment Outbreak sources: ground beef, petting zoos, fresh produce |
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0157:H7
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Produces shiga toxin
SLT-1 and SLT-2 (Stx1 and Stx2) Encoded on bacteriophage Has LEE pathogenicity island Locus of enterocyte effacement Attaching and effacing effect Loss of microvilli Also found in EPEC Severe abdominal cramping followed by watery and bloody diarrhea Fever frequently absent Hemolytic uremic syndrome (HUS) Occurs in 5-10% of individuals with EHEC Microangiopathic hemolytic anemia Organs become ischemic, esp. kidneys Laboratory diagnosis Streak sample on sorbitol-MacConkey agar PCR for genes encoding shiga toxin Enzyme immunoassays for shiga toxin in stool Treatment: supportive Antibiotics contraindicated Prevention Cook ground beef, wash hands |
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Enteropathogenic E. coli (EPEC)
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Leading cause of severe diarrhea in babies (<6 months) in developing countries
Pathogenesis: attaching and effacing effect on intestinal epithelial cells Results in loss of microvilli Causes watery diarrhea, can be severe Also vomiting, low grade fever Protracted disease causes malnutrition Breastfeeding is highly protective Inhibits adherence, contains protective antibodies against virulence factors |
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Enteroaggregative E. coli (EAEC)
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Typical stacked brick adherence pattern
Second most common cause of travelers’ diarrhea |
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Enteroinvasive E. coli (EIEC)
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Very similar to Shigella in pathogenesis and clinical presentation
Invade epithelial cells Microbial proteins take over the host actin-filament assembly Make cells rearrange their cytoskeletons Spread directly from cell to cell EPEC also usurps cytoskeleton to form adherent pedestals |
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shigellosis
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One of the most communicable bacterial diarrheas
Shigella appear to survive the low gastric pH Shigella (like EIEC) invade colonic epithelial cells Superficial infection confined to mucosa Invasion followed by intracellular multiplication, spread to adjacent cells, severe inflammation, and destruction of colonic mucosa Microabscesses coalesce to large abscesses that slough Inflammation and ulceration lead to abdominal pain and dysentery Invasiveness appears to be more important than shiga toxin One of the most communicable bacterial diarrheas Shigella appear to survive the low gastric pH Shigella (like EIEC) invade colonic epithelial cells Superficial infection confined to mucosa Invasion followed by intracellular multiplication, spread to adjacent cells, severe inflammation, and destruction of colonic mucosa Microabscesses coalesce to large abscesses that slough Inflammation and ulceration lead to abdominal pain and dysentery Invasiveness appears to be more important than shiga toxin Diagnosis Stool culture Fecal leucocytosis Stool assay for Shiga toxin Treatment Antibiotics shorten duration and decrease transmission Replace fluid losses Avoid antimotility agents Prevention Chlorinated water supply Hand washing Breast feeding |
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types of enteric infection:
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non-inflammatory: water diarrhea - no fecal WBC -
causes: ETEC, EPEC, EAEC, bacillus cereus Vibrio cholerae, C. perfringens, S. aureus, Giardia lamblia, Cryptosporidium parvum, and Norwalk-like viruses. Inflammatory also includes Vibrio parahemolyticus, Clostridium difficile, Campylobacter jejuni inflammatory: invasion cytotoxin, dysentery yes fecal leucocytes -- EHEC, salmonella enteritis, shigella penetrating systemic invasion enteric fever - yes WBC; salmonella typhi, yersinia |
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Patients with HLA-B27 antigen at risk for post-infection reactive arthritis = called:
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Reiter’s syndrome
Arthritis, uveitis, balanitis |
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Immunologic Complications of Enteric Infections
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Triggered by Shigella, Salmonella, Campylobacter, or Yersinia
Patients with HLA-B27 antigen at risk for post-infection reactive arthritis Reiter’s syndrome Arthritis, uveitis, balanitis Erythema nodosum |
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Salmonella Pathogenesis
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Salmonella ingested, pass to intestine
Several routes of intestinal invasion Through microfold (M) cells Bacterial mediated endocytosis Membrane ruffles engulf bacteria in large vesicles Disruption of tight junctions Typhoid fever: Bacteria pass through mucosa, enter Peyer’s patches Bacteria invade macrophages and disseminate Enterocolitis Intestinal invasion and neutrophil recruitment trigger inflammation Self-limited acute illness Incubation period 6 to 48 hours Nausea, vomiting, diarrhea Non-bloody stools Fevers, cramps, chills, headache Treatment Antibiotics only to at-risk persons May prolong duration of carriage |
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enteric fever:
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Enterocolitis with diarrhea not common
Usually resolves before onset of fever Low grade fever becomes high grade by second week Headache, malaise, chills, muscle pains Complications Neuropsychiatric (delirium, psychosis) Intestinal perforation Diagnosis: blood or bone marrow biopsy |
