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The Gram-Positive Bacilli of Medical Importance
Chapter 19 The Gram-Positive Bacilli of Medical Importance
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Medically Important Gram-Positive Bacilli
The gram-positive bacilli include about a dozen genera of medically significant bacteria They are differentiated on the basis of endospores, acid-fastness, and cell morphology
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Aerobic, Sporogenous Gram Positive Rods
Bacillus anthracis is the most prominent member of the genus Causative agent of antrax, a zoonosis that exists in both cutaneous and pulmonary forms
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Clinical significance - B
Clinical significance - B. anthracis = anthrax (seen primarily in cattle) Human infections follow exposure to infected animals or animal products - spores reside in soil & on plants Forms in humans Pulmonary - follows inhalation of spores; usually observed in workers in woolen mills (woolsorter’s disease) Cutaneous = malignant pustule - follows cutaneous inoculation of spores; lesion is small initially but enlarges with formation of black eschar; self-limiting Gastrointestinal = follows ingestion of contaminated food; begins with nausea, abdominal pain & vomiting followed by bloody diarrhea, toxemia & shock Septicemia - may follow any form
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Cutaneous antrax
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Epidemiology Habitat - spores in soil & on plants
Routes of transmission - aerosols, direct contact, ingestion Prevention & control - difficult; vaccine for susceptible individuals Treatment - penicillin
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Anaerobic, Sporogenous Gram Positive Rods
Clostridium C. tetani C. botulinum C. perfringens & other gas-producing clostridia C. difficile
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General characteristics
Gram positive, spore-forming rods - some are easily decolorized; cells are usually large; should be suspected if large cells (either gram + or -) seen in Gram stains Virulence factors Toxins Neurotoxins of C. botulinum & C. tetani Lethal toxins of C. perfringens - especially alpha toxin; actually a lecithinase Enterotoxin of C. perfringens & C. difficile Enzymes - numerous including hyaluronidase, collagenase, proteases, RNAse, DNAse, lecithinase
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Clinical manifestations: C. tetani - tetanus (lockjaw)
Toxic disease associated with 2 toxins – tetanospasmin (neurotoxin) & tetanolysin (hemolytic toxin) Spores of organism found in feces of humans & various animals; found in soil, dust - survive for years Incubation period = 1-54 days Signs & symptoms = cramps & twitching in muscles around wound, irritability, tachycardia & anxious facial expressions later progressing to lockjaw, spasms of the jaw and finally spasticity of neck, trunk & limbs
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Clinical manifestations: C. tetani - tetanus (lockjaw)
Spores enter body through wound contaminated with soil or feces - require relative deep wound to provide anaerobic conditions for sporulation & toxin formulation Toxin reaches CNS through blood, lymph or traveling through tissue spaces of peripheral nerves Neurotoxin blocks neurotransmitter release preventing muscle contraction when the opposing muscle contracts causing uncontrolled contraction of muscle
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Clinical manifestations: C. botulinum - botulism
Toxic disease associated with a neurotoxin - divides organisms into serogroups based on antigenic type of toxin Botulinum toxin is most powerful toxin known Acts on neuromuscular junctions of peripheral nervous system blocking release of nerve impulse causing a “flaccid (floppy)” paralysis Recovery of nerve function occurs only when new toxin-free nerve endings regenerated Antitoxin has no effect on bound only free toxin
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Clinical manifestations: C. botulinum - botulism
Foodborne botulism Follows ingestion of preformed toxin Foods most commonly involved = vegetables or condiments prepared from vegetables & fish (inadequately processed home-canned food is most common source in US) Nausea, vomitting & diarrhea are first clinical signs - neurologic symptoms usually appear hours after consumption of contaminated food characterized by descending paralysis that begins with ocular muscles (diplopia) rapidly progressing to pharyngeal muscles (dysphagia, hoarseness) & muscles of neck, trunk & limbs Death occurs through paralysis of respiratory muscles
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Clinical manifestations: C. botulinum - botulism
Infant botulism Follows ingestion of spores which germinate in intestine & produce toxin in intestine Foods most commonly involved - honey Only infants under 1 year are affected - no stable gut flora to inhibit germination of ingested spores Symptoms range from subclinical to death
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Clinical manifestations: C. botulinum - botulism
Wound botulism Follows contamination of a traumatic wound with organism or as complication of chronic drug abuse Toxin released, absorbed & travels via lymph & blood to nerve terminals Symptoms similar to foodborne botulism
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C. perfringens & other gas-producing clostridia
Anaerobic cellulitis Follows invasion of necrotic wound by proteolytic clostridia Characterized by gas accumulation, discoloration of underlying skin and presence of malodorous, brownish, purulent discharge
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C. perfringens & other gas-producing clostridia
Myonecrosis (gas gangrene) Involves invasion of normal healthy muscle surrounding traumatic wound Associated with deep wounds (e.g. warfare) containing foreign bodies, having blocked blood supplies and/or presence of necrotic tissue Symptoms include drowsiness, fever, tachycardia & a painful edematous wound with a sweet or foul-smelling discharge - gas is present but not as obvious as in cellulitis - may be fatal C. perfringens most common clostridial species involved
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C. difficile Associated with % of pseudomembranous enterocolitis following antimicrobial therapy especially following clindamycin, cephalosporins & ampicillin
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C. difficile Components of disease - disturbance of normal bowel flora by antimicrobial agents, a source of C. difficile (endogenous or exogenous) & organism must have potential for producing toxin Sources of C. difficile = hospital environment & endogenous (normal intestinal flora of 3% healthy adults and 10-20% hospitalized patients) Associated with two toxins - toxin A = enterotoxin causing diarrhea & toxin B = cytotoxin causing cellular damage
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Epidemiology Habitat Intestinal flora (C. perfringens, C. tetani & C. difficile) Environment - soil & animals Routes of transmission Traumatic wounds Ingestion Endogenous
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Epidemiology Prevention & Control Vaccine - tetanus toxoid (DPT)
Properly canning foods Avoid giving honey to child under 1 year (C. botulinum) Treatment Tetanus & botulism - specific antitoxin Debridement of wound Supportive therapy (respiratory assist) Antibiotic therapy (antibiogram)
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Gram-Positive Regular Non-Spore-Forming Bacilli
Non-spore-forming rods are divided among those that have regular and irregular shapes and staining properties Straight, nonpleomorphic rods stain evenly and include the genera Listeria and Erysipelothrix
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Listeria Species of medical importance - L. monocytogenes; only species pathogenic for man Clinical manifestations - restricted to several defined populations Neonates Early onset - acquired in utero or during birth Granulomatosis infantiseptica - fetus often stillborn; multiple granulomas Meningitis and sepsis Late onset - begins 2-3 weeks after birth; acquired from environment = meningitis and sepsis
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Listeria Pregnant women - puerperal sepsis & bacteremia
Immunocompromised - particularly with malignancies or renal transplant Meningitis - common cause in renal transplants Endocarditis Fatalities - greater in newborn under 4 weeks & adults over 50
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Epidemiology Natural habitat - primarily zoonotic but also found in soil, water, vegetation & intestine of humans Routes of transmission Ingestion - esp. milk products (not always killed by pasteurization), meat & cabbage Direct - female to infants or with environmental source Prevention and control - difficult (organisms are ubiquitous) Treatment - penicillin
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Erysipelothrix Species of medical importance - E. rhusiopathiae
Clinical manifestations Septicemia and endocarditis Uncommon but seen together when they occur Most susceptible = persons with previously damaged heart valves
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Erysipelothrix Erysipeloid
Inflammatory condition of skin; usually fingers & hands; suppuration Lesions usually erythematous with raised edge; spread peripherally Spontaneous cure = usual
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Epidemiology Natural habitat - ubiquitous; primarily zoonotic (mammals, birds, & fish); pigs = main source of human infection; also in soil where infected animals graze Modes of transmission = trauma (enter via abrasions); usually occupational (esp. butchers, meat processors, farmers, poultry workers, fisherman, vets) Prevention and control - protective clothing when handling infected sources Treatment - penicillin
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Gram-Positive Irregular Non-Spore-Forming Bacilli
Corynebacterium Species of medial importance C. diphtheriae C. ulcerans C. pseudotuberculosis Group JK
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Clinical manifestations - C. diphtheriae
Incubation period = 2-4 days Begins as pharyngitis (toxigenic & non-toxigenic strains) Only toxigenic strains produce pseudomembrane (toxin causes membrane; contains fibrin, WBC’s, cellular debris & bacteria - forms on pharynx but may extend into trachea); cervical adenitis common = bullneck appearance Uncomplicated diphtheria = resolves; membrane is coughed up
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Clinical manifestations - C. diphtheriae
Complications and mortality caused by respiratory obstruction or systemic effects of toxin Obstruction of airway due to membrane, edema & hemorrhage; can lead to sudden & complete suffocation - death Toxin may cause myocarditis (cardiac enlargement, weakness, arrhythmia & CHF) and paralysis of peripheral & cranial nerves (affected = soft palate, eyes & some muscles usually not serious unless diaphragm involved)
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Epidemiology Prevention and control - C. diphtheriae
Immunization with vaccine containing toxoid Schick test - uses intracutaneous injection of toxin; detects immune status Positive reaction = local edema, necrosis & desquamation = susceptible (no antitoxin) Negative reaction = no reaction = immune (toxin neutralized by circulating Ab = antitoxin)
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Epidemiology Treatment Antitoxin (antiserum)
Uses preformed Ab’s produced in horses or humans (hyperimmune IgG) Must be administered early before toxin attaches to target cells Hypersensitivity & serum sickness may result from horse serum & complicate therapy Antibiotics - penicillins & erythromycin Supportive therapy - removal of obstructions, minimize CHF, regulate respiration
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Mycobacteria General characteristics
Aerobic, non-sporogenous, non-motile rods Acid fast - cells resist acid decolorization Possess high levels of mycolic acids and other lipids in addition to peptidoglycan in their cell walls Slow growing (2 days - 6 weeks) Highly resistant to disinfectant & sterilization procedures
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Clinical Manifestations
M. leprae - Hansen's disease Chronic infectious disease - over 200 new cases diagnosed each year; approx. 13 million person infected world-wide Method of transmission from person-person unknown; depends on a susceptible host Children more susceptible than adults; males more than females Most persons probably cannot be infected by any means May be acquired through skin-skin contact or contact with nasal discharge
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M. leprae - Hansen's disease
Presents clinically in either of two major forms - form is dependent on adequacy of host's cell-mediated response Tuberculoid leprosy - usually self-limiting; may regress spontaneously; single skin lesions and nerve involvement producing patches of anesthesia most common feature (produced by inflammatory response to organisms); organisms are extremely rare in tissue
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M. leprae - Hansen's disease
Lepromatous leprosy - progressive & malignant; may be fatal; skin involvement extensive; organisms found in every organ - major changes detected in skin, nerves & testes; lesions of skin & mm - hypopigmented or nodular skin lesions common - nose deformities caused by destruction of cartilaginous septum by organisms; involvement of peripheral nerves not severe
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Staging of tuberculosis
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M. tuberculosis - occurs in 2 forms
Primary tuberculosis - seen in individuals who have never been exposed to organism Organisms enter host by several routes including skin, genitourinary tract, alimentary tract - most acquire through respiratory tract Inhaled organisms become deposited in alveoli of the lung and are phagocytized by alveolar macrophages where they multiply Organisms generally encounter little host resistance; are carried to lymph nodes through the lymphatics If organisms escape lymph nodes, enter the blood via the thoracic duct - are disseminated throughout the body producing numerous foci in various organs
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Primary TB Primary features of disease = tubercles & caseous necrosis
Tubercles formed when macrophages surround organisms forming elongated epithelioid cells arranged in concentric layers to form the granulomatous tubercles - tubercles are classically surrounded by lymphocytes & fibroblasts Caseous necrosis - characterized by disintegration of tubercle forming a coagulated, homogenous, cheeselike mass
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Progression of infection to disease depends on adequacy of CMI response - may be assisted by humoral response Good immune response - decreased multiplication of organisms, cessation of dissemination and healing of lesions by fibrosis & calcification (Ghon complex) - organisms may remain viable in these lesions for many years Poor immune response - progression to disease with liquification of caseous mass, rupture of tubercle lesion and spread of organisms to other parts of lung and body
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Secondary or reactivation tuberculosis
Occurs in persons who have been previously infected Associated with a breakdown in host’s cellular immune system (age, diabetes, obstructive pulmonary disease or other diseases) Localized lesion becomes necrotic and liquifies - may rupture into pulmonary vein and become disseminated to other body parts (miliary tb)
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Mycobacteria Other Than Tuberculosis (MOTT)
Pulmonary disease Organisms most commonly involved include M. kansasii & M. avium-intracellulare complex Usually occurs in middle-aged men with chronic lung disease Predisposing conditions = pneumoconiosis (coal miner’s disease), previous tb, chronic bronchitis, chronic obstructive lung disease, lung malignancy, AIDS
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Mycobacteria Other Than Tuberculosis (MOTT)
Skin & soft tissue infections Associated with M. fortuitum, M. chelonae, M. marinum & M. ulcerans M. fortuitum-chelonae complex cause local abscesses at site of injections or after trauma & surgical wounds, corneal infections after penetrating injury to eye and endocarditis after heart surgery M. ulcerans - cause a cutaneous ulcer called Bairnsdale (Australia) or Buruli (Africa) ulcer
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Mycobacteria Other Than Tuberculosis (MOTT)
M. marinum - found in fresh & salt water; cutaneous granulomas and ulcers associated with swimming pools (swimming pool granulomas) and aquariums (fish tank granulomas)
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Epidemiology Habitat M. leprae - humans constitute major source; armadillos recently implicated M. tuberculosis - humans constitute major source MOTT - environment (soil, plants, water) Transmission Leprosy - unclear; probably skin-skin contact or contact with nasal secretions - requires susceptible host (most humans not susceptible) Tuberculosis - aerosols most common mode; may also be acquired by ingestion or direct skin contact MOTT - human to human transmission not involved; requires contact with environmental source
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Control & prevention Leprosy - treatment of case contacts; long incubation period (3-10 years); isolation of known cases no longer necessary for more than 2 months
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Control & prevention Tuberculosis
Identification & treatment of infected persons Skin testing - tuberculin (purified protein derivative = PPD) injected subcutaneously; positive = exposure - not disease
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Control & prevention Xray evidence - calcified lesions may be evident as radiopaque area of lung Persons thought to be candidates for active diseases are treated for 1 year with INH
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Control & prevention Vaccine = BCG (Bacille of Calmette & Guerin); uses laboratory strain of M. bovis Widely used throughout the world to immunize negative tuberculin reactors Rarely used in US - primarily because successful immunization causes conversion of person to positive tuberculin test
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Treatment Leprosy - sulfones (esp. dapsone); infectivity disappears in 50 days may need to take drug for life Tuberculosis - isoniazid hydrazine (INH) = drug of choice; multiple resistance common today; known cases often treated with multiple drugs including streptomycin, rifampin, ethambutol & amikacin MOTT - usually highly resistant to drugs; often require surgical removal of lesions to treat
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