-
*Medically Important Gram-Positive BacilliCan be subdivided into
three general groups, based on presence or absence of endospores
and acid-fastnessThree general
groups:Endospore-formersNon-endospore-formersIrregular shaped and
staining properties
-
*
-
*Spore-Forming BacilliGenus BacillusGenus ClostridiumGenus
Sporolactobacillus
-
*General Characteristics of the Genus Bacillus Gram-positive,
endospore-forming, motile rodsMostly saprobicAerobic and catalase
positiveVersatile in degrading complex macromoleculesSource of
antibioticsPrimary habitat is soil2 species of medical
importance:Bacillus anthracisBacillus cereus
-
*Bacillus AnthracisLarge, block-shaped rodsCentral spores that
develop under all conditions except in the living bodyVirulence
factors polypeptide capsule and exotoxins3 types of
anthrax:Cutaneous spores enter through skin, black sore- eschar;
least dangerousPulmonary inhalation of sporesGastrointestinal
ingested spores
-
Cutaneous anthrax*
-
*Control and TreatmentTreated with penicillin, tetracycline, or
ciprofloxacinVaccines Live spores and toxoid to protect
livestockPurified toxoid; for high risk occupations and military
personnel; toxoid 6 inoculations over 1.5 years; annual
boosters
-
*Bacillus anthracis
-
*Bacillus CereusCommon airborne and dustborne; usual methods of
disinfection and antisepsis are ineffectiveGrows in foods, spores
survive cooking and reheatingIngestion of toxin-containing food
causes nausea, vomiting, abdominal cramps, and diarrhea; 24-hour
durationNo treatmentIncreasingly reported in immunosuppressed
-
*The Genus ClostridiumGram-positive, spore-forming rodsAnaerobic
and catalase negative120 speciesOval or spherical spores produced
only under anaerobic conditionsSynthesize organic acids, alcohols,
and exotoxinsCause wound infections, tissue infections, and food
intoxications
-
*
-
*Gas GangreneClostridium perfringens most frequent clostridia
involved in soft tissue and wound infections myonecrosisSpores
found in soil, human skin, intestine, and vaginaPredisposing
factors surgical incisions, compound fractures, diabetic ulcers,
septic abortions, puncture wounds, gunshot wounds
-
*Virulence FactorsVirulence factorsToxinsAlpha toxin causes RBC
rupture, edema, and tissue
destructionCollagenaseHyaluronidaseDNase
-
Growth of Clostridium perfringens*
-
*PathologyNot highly invasive; requires damaged and dead tissue
and anaerobic conditionsConditions stimulate spore germination,
vegetative growth and release of exotoxins, and other virulence
factorsFermentation of muscle carbohydrates results in the
formation of gas and further destruction of tissue
-
Myonecrosis*
-
*Treatment and PreventionImmediate cleansing of dirty wounds,
deep wounds, compound fractures, and infected incisionsDebridement
of disease tissueLarge doses of cephalosporin or
penicillinHyperbaric oxygen therapy No vaccines available
-
*Clostridium Difficile-Associated Disease (CDAD)Normal resident
of colon, in low numbersCauses antibiotic-associated colitis
Relatively non-invasive; treatment with broad-spectrum antibiotics
kills the other bacteria, allowing C. difficile to overgrowProduces
enterotoxins that damage intestinesMajor cause of diarrhea in
hospitalsIncreasingly more common in community-acquired
diarrhea
-
*Treatment and PreventionMild uncomplicated cases respond to
fluid and electrolyte replacement and withdrawal of
antimicrobialsSevere infections treated with oral vancomycin or
metronidazole and replacement culturesIncreased precautions to
prevent spread
-
Antibiotic-associated colitis*
-
*Tetanus Clostridium tetaniCommon resident of soil and GI tracts
of animals Causes tetanus or lockjaw, a neuromuscular diseaseMost
commonly among geriatric patients and IV drug abusers; neonates in
developing countries
-
*PathologySpores usually enter through accidental puncture
wounds, burns, umbilical stumps, frostbite, and crushed body
partsAnaerobic environment is required for vegetative cells to grow
and release toxinTetanospasmin neurotoxin causes paralysis by
binding to motor nerve endings; blocking the release of
neurotransmitter for muscular contraction inhibition; muscles
contract uncontrollably Death most often due to paralysis of
respiratory muscles
-
The events in tetanus*
-
Neonatal tetanus*
-
*Treatment and PreventionTreatment aimed at deterring degree of
toxemia and infection and maintaining homeostasisAntitoxin therapy
with human tetanus immune globulin; inactivates circulating toxin
but does not counteract that which is already boundControl
infection with penicillin or tetracycline; and muscle
relaxantsVaccine available; booster needed every 10 years
-
*Clostridial Food PoisoningClostridium botulinum rare but severe
intoxication usually from home canned foodClostridium perfringens
mild intestinal illness; second most common form of food poisoning
worldwide
-
*Botulinum Food PoisoningBotulism intoxication associated with
inadequate food preservationClostridium botulinum spore-forming
anaerobe; commonly inhabits soil and water
-
*PathogenesisSpores are present on food when gathered and
processedIf reliable temperature and pressure are not achieved air
will be evacuated but spores will remainAnaerobic conditions favor
spore germination and vegetative growthPotent toxin, botulin, is
releasedToxin is carried to neuromuscular junctions and blocks the
release of acetylcholine, necessary for muscle contraction to
occurDouble or blurred vision, difficulty swallowing, neuromuscular
symptoms
-
Physiological effects of botulism toxin*
-
*Infant and Wound BotulismInfant botulism caused by ingested
spores that germinate and release toxin; flaccid paralysisWound
botulism spores enter wound and cause food poisoning symptoms
-
*Treatment and PreventionDetermine presence of toxin in food,
intestinal contents or fecesAdminister antitoxin; cardiac and
respiratory supportInfectious botulism treated with
penicillinPractice proper methods of preserving and handling canned
foods; addition of preservatives
-
*Clostridial GastroenteritisClostrium perfringensSpores
contaminate food that has not been cooked thoroughly enough to
destroy sporesSpores germinate and multiply (especially if
unrefrigerated)When consumed, toxin is produced in the intestine;
acts on epithelial cells, acute abdominal pain, diarrhea, and
nauseaRapid recovery
-
*
-
*Gram-Positive Regular Non-Spore-Forming BacilliRegular: stain
uniformly and do not assume pleomorphic shapesMedically
important:Listeria monocytogenesErysipelothrix rhusiopathiae
-
*Listeria MonocytogenesNon-spore-forming gram-positive Ranging
from coccobacilli to long filaments1-4 flagellaNo capsulesResistant
to cold, heat, salt, pH extremes, and bileVirulence attributed to
ability to replicate in the cytoplasm of cells after inducing
phagocytosis; avoids humoral immune system
-
*Multiplication cycle of Listeria monocytogenes
-
*Epidemiology and PathologyPrimary reservoir is soil and water;
animal intestinesCan contaminate foods and grow during
refrigerationListeriosis most cases associated with dairy products,
poultry, and meat Often mild or subclinical in normal adults
Immunocompromised patients, fetuses, and neonates; affects brain
and meninges20% death rate
-
*Diagnosis and ControlCulture requires lengthy cold enrichment
processRapid diagnostic tests using ELISA, immunofluorescence, and
DNA analysisAmpicillin and trimethoprim/ sulfamethoxazolePrevention
pasteurization and cooking
-
*Gram-Positive Irregular Non-Spore-Forming BacilliIrregular:
pleomorphic, stain unevenlyMedically important
genera:CorynebacteriumPropionibacteriumMycobacteriumActinomycesNocardia
-
*20 genera; Corynebacterium, Mycobacterium, and Nocardia
greatest clinical significanceAll produce catalase, possess mycolic
acids, and a unique type of peptidoglycan
-
*Corynebacterium DiptheriaeGram-positive irregular bacilli
-
*EpidemiologyReservoir of healthy carriers; potential for
diphtheria is always presentMost cases occur in non-immunized
children living in crowded, unsanitary conditionsAcquired via
respiratory droplets from carriers or actively infected
individuals
-
*Incidence and case fatality of diphtheria
-
*Pathology2 stages of disease: Local infection upper respiratory
tract inflammation Sore throat, nausea, vomiting, swollen lymph
nodes; pseudomembrane formation can cause asphyxiation
Diptherotoxin production and toxemia Target organs primarily heart
and nerves
-
The Iditirod
-
*Diagnostic MethodsPseudomembrane and swelling
indicativeStainsConditions, historySerological assay
-
Diagnosing diphtheria*
-
*Treatment and PreventionAntitoxinPenicillin or
erythromycinPrevented by toxoid vaccine series and boosters
-
*Genus PropionibacteriumPropionibacterium acnes most
commonGram-positive rodsAerotolerant or anaerobicNontoxigenicCommon
resident of pilosebaceous glandsCauses acne
-
*Mycobacteria: Acid-Fast BacilliGram-positive irregular
bacilliAcid-fast stainingStrict aerobes Produce catalasePossess
mycolic acids and a unique type of peptidoglycanDo not form
capsules, flagella, or sporesGrow slowly
-
*
-
Microscopic morphology of mycobacteria*
-
*Mycobacterium TuberculosisTubercle bacillusProduces no
exotoxins or enzymes that contribute to infectiousnessVirulence
factors contain complex waxes and cord factor that prevent
destruction by lysosomes or macrophages
-
*Epidemiology of Tuberculosis Predisposing factors include:
inadequate nutrition, debilitation of the immune system, poor
access to medical care, lung damage, and geneticsEstimate 1/3rd of
world population and 15 million in U.S. carry tubercle bacillus;
highest rate in U.S. occurring in recent immigrantsBacillus very
resistant; transmitted by airborne respiratory droplets
-
*Course of Infection and Disease5% to 10% of infected people
develop clinical diseaseUntreated, the disease progresses slowly;
majority of TB cases contained in lungsClinical tuberculosis
divided into:Primary tuberculosisSecondary tuberculosis
(reactivation or reinfection)Disseminated (extrapulmonary)
tuberculosis
-
Staging of tuberculosis*
-
*Primary TBInfectious dose 10 cellsPhagocytosed by alveolar
macrophages and multiply intracellularlyAfter 3-4 weeks immune
system attacks, forming tubercles, granulomas consisting of a
central core containing bacilli surrounded by WBCs tubercleIf
center of tubercle breaks down into necrotic caseous lesions, they
gradually heal by calcification
-
Section of a tubercle*
-
*Secondary TBIf patient doesnt recover from primary
tuberculosis, reactivation of bacilli can occurTubercles expand and
drain into the bronchial tubes and upper respiratory tractGradually
the patient experiences more severe symptomsViolent coughing,
greenish or bloody sputum, fever, anorexia, weight loss,
fatigueUntreated, 60% mortality rate
-
*Extrapulmonary TBDuring secondary TB, bacilli disseminate to
regional lymph nodes, kidneys, long bones, genital tract, brain,
and meningesThese complications are grave
-
*Diagnosis In vivo or tuberculin testingMantoux test local
intradermal injection of purified protein derivative (PPD); look
for red wheal to form in 48-72 hours induration; established
guidelines to indicate interpretation of result based on size of
wheal and specific population factorsX-raysDirect identification of
acid-fast bacilli in specimenCultural isolation and biochemical
testing
-
*Skin testing for tuberculosis
-
X-ray of secondary tubercular infection*
-
Fluorescent acid-fast stain of Mycobacterium tuberculosis*
-
*Management and Prevention of TB6-24 months of at least 2 drugs
from a list of 11One pill regimen called Rifater (isoniazid,
rifampin, pyrazinamide)Vaccine based on attenuated bacilli
Calmet-Guerin strain of M. bovis used in other countries
-
*Mycobacterium Leprae: The Leprosy Bacillus Hansens
bacillus/Hansens DiseaseStrict parasite has not been grown on
artificial media or tissue cultureSlowest growing of all
speciesMultiplies within host cells in large packets called
globiCauses leprosy, a chronic disease that begins in the skin and
mucous membranes and progresses into nerves
-
*Epidemiology and Transmission of LeprosyEndemic regions
throughout the worldMechanism of transmission is not fully
verifiedNot highly virulent; appears that health and living
conditions influence susceptibility and the course of the
diseaseMay be associated with specific genetic marker
-
Leprosy lesions*
-
*Course of Infection and DiseaseMacrophages phagocytize the
bacilli, but a weakened macrophage or slow T cell response may not
kill bacillusIncubation from 2-5 years; if untreated, bacilli grow
slowly in the skin macrophages and Schwann cells of peripheral
nerves2 forms possible:Tuberculoid asymmetrical, shallow lesions,
damage nerves results in local loss of pain receptionLepromatous a
deeply nodular infection that causes severe disfigurement of the
face and extremities, widespread dissemination
-
*
-
*DiagnosingCombination of symptomology, microscopic examination
of lesions, and patient historyNumbness in hands and feet, loss of
heat and cold sensitivity, muscle weakness, thickened earlobes,
chronic stuffy noseDetection of acid-fast bacilli in skin lesions,
nasal discharges, and tissue samples
-
Feather test for leprosy*
-
*Treatment and PreventionTreatment by long-term combined
therapyPrevention requires constant surveillance of high-risk
populationsWHO sponsoring a trial vaccine
-
*Infections by Non-Tuberculosis Mycobacteria (NTM)M. avium
complex third most common cause of death in AIDS patientsM. kansaii
pulmonary infections in adult white males with emphysema or
bronchitisM. marinum water inhabitant; lesions develop after
scraping on swimming pool concreteM. scrofulaceum infects cervical
lymph nodesM. paratuberculosis raw cows milk; recovered from 65% of
individuals diagnosed with Crohns disease
-
Chronic swimming pool granuloma*
-
*
-
*Actinomycetes: Filamentous BacilliGenera Actinomyces &
Nocardia are nonmotile filamentous bacteria related to
mycobacteriaMay cause chronic infection of skin and soft
tissuesActinomyces israelii responsible for diseases of the oral
cavity, thoracic or intestines actinomycosesNocardia brasiliensis
causes pulmonary disease similar to TB
-
Symptoms and signs of actinomycosis*
-
Nocardiosis*
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