1
Approach to Infectious Diseases and their prevention
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2
Antibiotic stewardship practices
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3Community-Acquired Infections
4
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Health Care?Associated Infections
5
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Gram-Positive Bacteria (part-1)6
Gram-Positive Bacteria (part-2)
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7
Gram-Negative Bacteria (part-1)
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8Gram-Negative Bacteria (part-2)
9
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Spirochetal Diseases
10
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Diseases Caused by Atypical/Miscellaneous Bacterial Infections11
Revision-cum-exam on bacteria (Must to know type)
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12
Infections Due to DNA Viruses
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113
Infections Due to RNA Viruses (part 1)
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14
Infections Due to RNA Viruses (part 2)
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15HIV/AIDS ? part 1
16
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HIV/AIDS ? part 2
17
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Fungal Infections18
Parasitic Infections (part 1)
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19
Parasitic Infections (part 2)
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20Revision-cum-exam on Virus, Fungal, and Parasite (Must to know type)
DIPHTHERIA
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Listeria
Clostridial Infections
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TetanusBotulism
Gas gangrene
DIPHTHERIA
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Nasopharyngeal and skin infection caused by Corynebacterium diphtheriaeToxigenic strains most frequently cause pharyngeal diphtheria, nontoxigenic
strains commonly cause cutaneous disease
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Cutaneous diphtheria is usually a secondary infection after primary skin lesionsdue to trauma, allergy, or autoimmunity
In tropical latitudes, cutaneous diphtheria is more common than respiratory
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diphtheria
In temperate climate, Pharyngeal one is most common during winter months
Risk factors for diphtheria outbreaks include older age, lack of vaccination,
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alcoholism, low socioeconomic status, crowded living conditions
Carriers are defined as individuals who have positive cultures for C.
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diphtheriae and who either are asymptomatic or have symptoms but lackpseudomembranes
ETIOPATHOGENESIS
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Unencapsulated, nonmotile, and nonsporulating with club-shaped bacillary
appearance and typically form palisades, known as "Chinese characters"
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The specific laboratory media using tellurite, colistin, or nalidixic acidPhenotypes:- nontoxigenic (tox?) and toxigenic (tox+) using corynebacteriophages
Under iron-limiting conditions leads to the optimal expression
Transmitted via the aerosol route, with only human reservoirs, IP-2?5 days
Diphtheria toxin is the primary virulence factor and is taken up in the bloodstream,
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from which it is distributed to all organ systems in the body
In vitro, the toxin may be separated into two chains by digestion with serine
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proteases: the N-terminal A fragment and the C-terminal B fragmentDelivery of the A fragment into the eukaryotic cell cytosol results in irreversible
inhibition of protein synthesis by NAD+-dependent ADP-ribosylation of elongation
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factor 2
Pathologic findings of diphtheria include mucosal ulcers with a pseudomembranous
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coating composed of an inner band of fibrin and a luminal band of neutrophilsCLINICAL MANIFESTATIONS
Should be considered when a patient has severe pharyngitis, particularly when there
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is difficulty swallowing, respiratory compromise, or signs of systemic disease (e.g.,myocarditis or generalized weakness)
Clinical diagnosis of diphtheria is IF sore throat; pseudomembranous lesions; and low-
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grade fever
Most commonly, the pseudomembranous lesion is located in the tonsillopharyngeal
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regionIt is gray or whitish, sharply demarcated, tightly adherent to the underlying tissues
(Unlike streptococcal pharyngitis)
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Massive swelling of the tonsils and may present with "bul -neck" diphtheria
Polyneuropathy (3?5 weeks after) and myocarditis are late toxic manifestations
Cranial nerve dysfunction typically precedes other neuropathy and typically
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reversible in patients who survive the acute phaseOther complications include pneumonia, renal failure, encephalitis, cerebral
infarction, pulmonary embolism, and serum sickness from antitoxin therapy
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Cutaneous Diphtheria IS characterized by punchedout ulcerative lesions with
necrotic sloughing or pseudomembrane formation
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DiagnosisThe diagnosis of diphtheria is based on clinical signs and symptoms plus
laboratory confirmation
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Laboratory diagnosis of diphtheria is based either on cultivation or on the
demonstration of local lesions with characteristic histopathology
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A diagnosis of cutaneous diphtheria requires laboratory confirmation sincethe lesions are not characteristic and are indistinguishable from other
dermatoses
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TreatmentPatients in whom diphtheria is suspected should be hospitalized in respiratory
isolation rooms, with close monitoring of cardiac and respiratory function
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Once a clinical diagnosis of diphtheria is made, diphtheria antitoxin should be
administered as rapidly as possible after a test dose
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Antibiotics are used in the management of diphtheria primarily to preventtransmission to susceptible contacts
Procaine penicillin G, 600,000 U IM q12h until the patient can swallow
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comfortably; then oral penicillin V, 125?250 mg qid to complete a 14-day
course (or Erythromycin, 500 mg IV q6h, rifampin and clindamycin)
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For patients in whom the organism is not eradicated after a 14-day course oferythromycin or penicillin, an additional 10-day course followed by repeat
culture is recommended
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Patients who recover from diphtheria should receive the appropriate vaccine if
diphtheria antitoxin titer of <0.01 U/mL
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Prognosis and preventionRisk factors for death include
bullneck diphtheria;
myocarditis with ventricular tachycardia;
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atrial fibrillation;complete heart block;
an age of >60 years or <6 months;
alcoholism;
extensive pseudomembrane elongation;
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laryngeal, tracheal, or bronchial involvementInterval between the onset of local disease and the administration of antitoxin
DTaP is currently recommended for children up to the age of 7
It is recommended that all adults receive a single dose of Tdap if they have not received it previously,
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regardless of the interval since the last dose of Td (tetanus and reduced-dose diphtheria toxoids,
adsorbed); after that decennial Td booster
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Close contacts of diphtheria patients should undergo throat culture and After samples for throatculture obtained, antimicrobial prophylaxis should be considered for all contacts (7?10 days of oral
erythromycin or one dose of IM benzathine penicil in G, 1.2 mil ion units for persons 6 years of age)
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OTHER CORYNEBACTERIAL INFECTIONSNondiphtherial corynebacteria, referred to as diphtheroids or coryneforms,
are frequently considered colonizers or contaminants; however, they have
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been associated with invasive disease, particularly in immunocompromised
patients
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Humans are the natural reservoirs for several coryneforms, including C.xerosis, C. pseudodiphtheriticum, C. striatum, C. minutissimum, C. jeikeium,
C. urealyticum, and Arcanobacterium haemolyticum
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Animal reservoirs are responsible for carriage of Arcanobacterium
pyogenes, C. ulcerans, and C. pseudotuberculosis
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Soil is the natural reservoir for Rhodococcus equiListeria monocytogenes Infections
L. monocytogenes is of interest not only to clinicians but also to basic scientists as
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a model intracellular pathogen that is used to study
A food-borne pathogen that can cause serious infections, particularly in
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pregnant women and immunocompromised individualsBroad host range of reservoirs, facultatively anaerobic, nonsporulating, motile,
grows over a broad temperature range
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Commonly found in processed and unprocessed foods of animal and plant
origin
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Like other enteric pathogens, L. monocytogenes induces its own internalizationby cells that are not normal y phagocytic
Weakly -hemolytic (an essential determinant of its pathogenicity, listeriolysin O
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Expresses a surface protein, ActA, an essential actin-based motility system (Otherpathogens like Shigella, Mycobacterium, Rickettsia, and Burkholderia species
use a related pathogenic strategy that allows cell-to-cell spread)
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There is an inverse relationship between toxicity and virulence--i.e., the more
cytotoxic the strain, the less virulent it is in animals
Symptoms/diagnosis/treatment
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Symptoms overlap greatly with those of other infections
It presents with several clinical syndromes (meningitis and septicemia are most
common)
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Listerial gastroenteritis typically develops within 48 h of ingestion of a large
inoculum of bacteria
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A nonspecific flulike il ness with fever is a common presentation in pregnantwomen F/B myalgias, arthralgias, backache, and headache
Granulomatosis infantiseptica is an overwhelming fetal infection with miliary
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microabscesses and granulomas
It should be considered in all older or chronically ill adults with "aseptic"
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meningitis (frequently subacute)The diagnosis is typically made by culture of blood, cerebrospinal fluid (CSF), or
amniotic fluid
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Ampicil in is the drug of choice with/out Gentamycin
Clostridial Infections
They are pleomorphic, gram variable, mostly motile (except C. perfringens, C.
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ramosum, and C. innocuum, with variable oxygen tolerance
Produce more protein toxins than any other bacterial genus, including
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neurotoxins, enterotoxins, cytotoxins, collagenases, permeases, necrotizingtoxins, lipases, lecithinases, hemolysins, proteinases, hyaluronidases, DNases,
ADPribosyltransferases, and neuraminidases
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C. tetani and C. botulinum, cause specific clinical disease by elaborating single
toxin while, C. perfringens and C. septicum cause aggressive necrotizing
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infections due to multiple toxinsBotulinum and tetanus neurotoxins are the most potent (LD- 0.2?10 ng/kg)and
Epsilon toxin of C. perfringens is the most lethal one (used as agent of
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bioterrorism)
Widespread in nature, forming endospores, Commensals in the intestinal tract of
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humans and animals, in the female genital tract, and on the oral mucosa (notal commensal clostridia are toxigenic)
Tetanus
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"The acute onset of hypertonia or ... painful muscular contractions (usually of themuscles of the jaw and neck) and generalized muscle spasms without other apparent
medical cause"... CDC
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Maternal tetanus is defined by the WHO as tetanus occurring during pregnancy or
within 6 weeks after the conclusion of pregnancy (whether wit
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The spores or bacteria enter the body through abrasions, wounds, or (in the case ofneonates) the umbilical stump.h birth, miscarriage, or abortion)
In 20?30% of cases of tetanus, no puncture entry wound is found
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Higher risks in old age, Injection drug users, and incomplete vaccinationOnly those bacteria producing tetanus toxin (tetanospasmin) can cause tetanus
Although closely related to the botulinum toxins in structure and mode of action,
tetanus toxin undergoes retrograde transport into the central nervous system and thus
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produces different clinical effects
Unlike other components of the endosomal contents, which undergo acidification
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following internalization, tetanus toxin is transported in a carefully regulated pH-neutral environment that prevents an acid induced conformational change
Prevents transmitter release and effectively blocks inhibitory interneuron discharge
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CLINICAL MANIFESTATIONS
Broadly divided into generalized (including neonatal) and local
Muscles of the face and jaw often are af ected first
The incubation period and the period of onset are of particular
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significance; shorter times are associated with worse outcome
The commonest initial symptoms are trismus (lockjaw), muscle pain and
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stiffness, back pain, and difficulty swallowingAutonomic disturbance is maximal during the second week of severe
tetanus, and death occurs due to cardiovascular events
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DIAGNOSIS
The diagnosis of tetanus is based on clinical findings
Culture of C. tetani from a wound provides supportive evidence
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Serum anti-tetanus immunoglobulin G may also be measured in a sampletaken before the administration of antitoxin or immunoglobulin; levels >0.1
IU/mL are deemed protective and do not support the diagnosis of tetanus
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D/D- strychnine poisoning and dystonic reactions to antidopaminergic
drugs ? Episodic nature
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TREATMENT
Management strategies aim to neutralize remaining unbound toxin and support
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vital functions until the effects of the toxin have worn offPatients should be nursed in calm, quiet environments because light and noise
can trigger spasms
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Entry wound should be identified, cleaned, and debrided of necrotic material
Metronidazole (400mg rectally or 500 mg IV every 6 h for 7 days) is the preferred
antibiotic; Or penicillin, although this may exacerbate spasms
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TIG is the preparation of choice (less likely to be associated with anaphylactoid
reactions); 3000?5000 IU as a single IM dose, a portion should be injected
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around the wound; nowadays 50?1500 IU administered intrathecal y alsoEquine derived antitoxin (available widely), 10,000?20,000U, after testing for
hypersensitivity
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Spasms are controlled by heavy sedation with benzodiazepines
Cardiovascular stability (dif icult to treat) is improved by increasing sedation with
IV magnesium sulfate, morphine, or other sedatives
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Patients must be given a full primary course of immunization
Prevention
Good wound care and immunization
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Individuals sustaining tetanus-prone wounds should be immunized iftheir vaccination status is incomplete or unknown or
if their last booster was given >10 years earlier
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Patients sustaining wounds not classified as clean or minor should also
undergo passive immunization with TIG
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BotulismIngestion of botulinum toxin in contaminated food (food-borne botulism)
Wound botulism
Infant botulism
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Adult intestinal colonization botulismBotulism symptoms have been reported in patients receiving injections of
botulinum toxin for cosmetic or therapeutic purposes (iatrogenic botulism;
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Moreover, botulism was reported after inhalation of botulinum toxin in alaboratory setting
Intentional Botulism
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PathogenesisConsumption of home-preserved fish or vegetable products main source
Seven serologically distinct confirmed serotypes of botulinum toxin (A
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through G); Human cases associated with serotypes A, B, E, and FFour recognized species of clostridia: Clostridium botulinum, Clostridium
argentinense, Clostridium baratii, and Clostridium butyricum
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Neurotoxin enters the vascular system and is transported to peripheral
cholinergic nerve terminals, including neuromuscular junctions,
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postganglionic parasympathetic nerve endings, and peripheral gangliawith Inhibition of acetylcholine release
CLINICAL MANIFESTATIONS
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All forms of botulism manifest as a relatively distinct clinical syndrome of
symmetric cranial-nerve palsies followed by descending bilateral flaccid
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paralysis of voluntary muscles, which may progress to respiratorycompromise and death
Weakness descends, often rapidly, from the head to involve the neck, arms,
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thorax, and legs; occasionally, weakness is asymmetric
In some instances, unfortunately, the severe ptosis, expressionless face, and
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weak phonation of patients with botulism have been interpreted as signs ofmental status changes due to alcohol intoxication, drug overdose,
encephalitis, or meningitis--a conclusion that delays an accurate diagnosis
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DIAGNOSISDiagnosed primarily on clinical grounds, with laboratory confirmation by specific tests that
identify botulinum toxin in clinical and food samples (mouse bioassay, BEST METHOD)
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The temporal occurrence of two or more cases with symptoms compatible with botulism isessentially pathognomonic because other illnesses that resemble botulism do not usually occur
in clusters
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Food history and the names of contacts who may have shared foods should be obtained
before illness progresses
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Ascertainment of the patient's behavioral history related to injection drug use is criticalA history of recent abdominal surgery or antibiotic use may be important in the diagnosis of
adult intestinal colonization botulism
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D/D-Guil ain-Barre syndrome (GBS),
myasthenia gravis,
stroke syndromes,
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Eaton-Lambert syndrome,tick paralysis
poisoning by tetrodotoxin, shel fish, or
a host of rarer agents and antimicrobial drug?associated paralysis
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TREATMENTMeticulous intensive care and immediate administration of botulinum
antitoxin (Botulism Antitoxin Heptavalent OR Botulism Immune Globulin
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Intravenous)Persons of all ages (including infants) in whom botulism is suspected should
be hospitalized immediately
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Suspect wounds and abscesses should be cleaned, debrided, and drained
promptly. The role of penicillin and metronidazole in treatment and
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decolonization is unclearPOLYMICROBIAL INFECTIONS INVOLVING
CLOSTRIDIA
In the absence of devitalized tissue, the presence of clostridia does not
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necessarily lead to infection (CLOSTRIDIAL WOUND CONTAMINATION)
It may appear in association with non-spore-forming anaerobes and facultative
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or aerobic organismsOften associated with severe local inflammation but may lack the characteristic
systemic signs of toxicity and rapid progression seen in other clostridial infections
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The treatment of mixed aerobic/anaerobic infection of the abdomen, perineum,
or gynecologic organs should be based on Gram's staining, culture, and
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antibiotic sensitivity informationAmpicillin or ampicillin/sulbactam combined with either clindamycin or
metronidazole is DOC
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ENTERIC CLOSTRIDIAL INFECTIONS
Illness results from the ingestion of food containing at least ~1 Billion viable vegetative
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cells, which sporulate and produce enterotoxinThe diarrhea develops within 7?30 h of ingestion is generally mild and self-limiting;
however, in the very young, the elderly, and the immunocompromised, symptoms
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are more severe and occasionally fatal
Enterotoxin-producing C. perfringens type A has been implicated and has been
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considered to play a role in antibiotic-associated diarrhea withoutpseudomembrane
Enteritis necroticans (gas gangrene of the bowel) is caused by toxin and toxin
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(Pathogenic) producing strains of C. perfringens type C
Necrotizing enterocolitis, associated with C. perfringens type A, in previously healthy
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adults AND low-birth-weight (premature) infants hospitalized in neonatal intensivecare units, af ects ileum in contrast to jejunum in enteritis necroticans
They should undergo nasogastric suction and receive IV fluids; Pyrantel is given by
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mouth, and the bowel is rested by fasting; Benzylpenicillin (1 mU) IV every 4 h, and
the patient is observed for complications requiring surgery
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Surgical indications; gas in the peritoneal cavity, absent bowel sounds, reboundtenderness, abdominal rigidity; however, the mortality rate ranges from 35% to 100%
CLOSTRIDIAL BACTEREMIA
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By C. perfringens and C. tertium mostly, rarely C. septicumC. tertium can be found in patients with malignancy or acute pancreatitis,
with or without neutropenic enterocolitis; and is resistant to metronidazole,
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clindamycin, and cephalosporinsPositive C. septicum patients have some association with gastrointestinal
anomaly or underlying malignancy and in addition, with neutropenia of any
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origin--and, more specifically, with neutropenic enterocolitis
Anaerobic blood cultures and Gram's stain interpretation remain the best
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diagnostic testsCLOSTRIDIAL SKIN AND SOFT-TISSUE
INFECTIONS
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Necrotizing clostridial soft-tissue infections; Severe pain, crepitus, brawny indurationwith rapid progression to skin sloughing, violaceous bul ae, and marked tachycardia
are characteristics
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Traumatic gas gangrene: conditions predisposing include crush-type injury,
laceration of large or medium-sized arteries, and open fractures of long bones that
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are contaminated with soil or bits of clothing containing the bacterial spores with IP-6 h <4 days
Diagnosis is not difficult because the infection always begins at the site of significant
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trauma, is associated with gas in the tissue, and is rapidly progressive Non-
inflammatory nature
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Spontaneous (nontraumatic) gas gangrene: occurs via hematogenous seeding ofnormal muscle with histotoxic from a gastrointestinal tract portal of entry
The first symptom may be confusion followed by the abrupt onset of excruciating
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pain in the absence of trauma, along with fever, should heighten suspicion
THEY should undergo aggressive diagnostic studies to rule out gastrointestinal
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pathologySurgical exploration, Gram's staining, blood culture, and histopathologic
examination are main stay of diagnosis and treatment
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Thank you