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)
NEISSERIA
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ENTEROBACTERIACEAE
PSEUDOMONADS
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BRUCELLA(E. coli, Klebsiella,
Proteus, Enterobacter)
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HAEMOPHILUS
SALMONELLA
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ACINETOBACTERFRANCISELLA
LEGIONELLA
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SHIGELLA
HELICOBACTER
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YERSINIABORDETELLA
VIBRIO
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CAMPYLOBACTER
BARTONELLA
NEISSERIA (N. meningitis & N. gonorrhoeae; IP-2-7days)
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N. meningitis; diplococcus that colonizes in the nasopharynx of healthy
adolescents and adults, use glucose and maltose to produce acid
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N. gonorrhoeae; grow on selective media and to use glucose but not maltose,sucrose, or lactose
Meningococci invasive disease are usually encapsulated with polysaccharide,
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and the antigenic nature of the capsule determines an organism's serogroup
Under capsule, an outer phospholipid membrane containing lipopolysaccharide
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(LPS, endotoxin) and multiple outer-membrane proteins (serotype)Gonococcus contains, on average, three genome copies per coccal unit; this
polyploidy permits a high level of antigenic variation and the survival of the
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organism in its host and resistant to antibiotics
Outer-Membrane Proteins (PILLI, OPA, PORIN, etc) and lipooligosaccharide
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(LOS): gonococcal structures that interact with epithelial cells, host factors seemto be important in mediating entry of gonococci into nonphagocytic cells (e.g.
complement deficiency)
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There are several patterns of disease: epidemic, outbreak, hyperendemic, and
sporadic or endemic
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Clusters of cases occur where there is an opportunity for increased transmission--i.e., in (semi-)closed communities
Smoking, crowding, and respiratory viral infection increase the risk of
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carriage/disease
Endothelial injury is central to many clinical features of meningococcemia,
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including increased vascular permeability, pathologic changes in vascular tone,loss of thromboresistance, intravascular coagulation, and myocardial dysfunction
Most common clinical syndromes are meningitis and meningococcal septicemia
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MENINGITIS: While 30?50% of patients present with a meningitis syndrome aloneOR up to 40% with some features of septicemia
SEPTICEMIA: alone accounts for up to 20% of cases
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CHRONIC MENINGOCOCCEMIA, presents as repeated episodes of petechial rashassociated with fever, joint pain/arthritis, and splenomegaly that may progress to
acute meningococcal septicemia if untreated
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POSTMENINGOCOCCAL REACTIVE DISEASE, an immune complex disease develops
~4?10 days after the onset of meningococcal disease
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Usually initially blanching in nature and indistinguishable from viral rashes, HOWEVER,
petechial or frankly purpuric over the hours after onset, THEN purpura fulminans
(fewer than <10% of children of all rashes) ? (occurs in two-thirds of Meningococcal cases)
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Clinical grounds and lab confirmation (blood cultures are positive in up to 75%
of cases, (PCR) analysis of whole-blood samples, lumbar puncture
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Third-generation cephalosporin, treated for 7 days10% DEATH, most common complication 10% of cases) is scarring after necrosis
of purpuric skin lesions
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Factors associated with a poorer prognosis are shock; young age (infancy),old age, and adolescence; coma; purpura fulminans; disseminated
intravascular coagulation; thrombocytopenia; leukopenia; absence of
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meningitis; metabolic acidosis; low plasma concentrations of antithrombin and
proteins S and C; high blood levels of PAI-1; and a low erythrocyte
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sedimentation rate or C-reactive protein levelPREVENTION;
1. Immunization- Polysaccharide Vaccines/Conjugate Vaccines/Vaccines Based
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on Subcapsular AntigensA monovalent serogroup A vaccine, manufactured in India, was licensed in 2010
and rol ed out to countries in the sub-Saharan African meningitis belt
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Chemoprophylaxis- Rifampin/Ceftriaxone as a single IM or
IV/Ciprofloxacin/ofloxacin
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GONORRHEA
Gonorrhea is a sexually transmitted infection (STI) of epithelium and commonly
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manifests as cervicitis, urethritis, proctitis, and conjunctivitisGonococcal Infections in Men
Gonococcal Infections in Women
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Acute urethritis
Cervicitis
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(more acute and intense than thoseof chlamydial cervicitis)
Epididymitis/prostitis
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Urethritis
Balanitis or further deep complications
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Vaginitisincluding abscesses
(occur in anestrogenic
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Women)
Anorectal Gonorrhea
Pharyngeal Gonorrhea
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Ocular GonorrheaGonorrhea in Pregnant Women, Neonates, and Children
Gonococcal Arthritis (DGI)
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Menstruation is a risk factor for dissemination, and two-thirds cases are in womenBacteremic stage and a joint-localized stage with suppurative arthritis
D/D; reactive arthritis AND septic arthritis
Rapid diagnosis - Gram's staining of urethral exudates
Nucleic acid probe tests are being substituted for culture, BUT NOT
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LEGALLY
Single IM dose of the third-generation cephalosporin, mainstay of
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therapyOR azithromycine (1g single dose)
Because co-infection with C. trachomatis occurs frequently, initial
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treatment regimens must also incorporate an agentDGI require higher dosages and longer durations of therapy
All persons who experience more than one episode of DGI should be
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evaluated for complement deficiencyCondoms, if properly used, effective protection against the transmission
and acquisition of gonorrhea
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Patients should be instructed to abstain from sexual intercourse until
therapy is completed and until they and their sex partners no longer
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have symptomHAEMOPHILUS
Grows both aerobical y (requires two factors: hemin (X factor) and nicotinamide
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adenine dinucleotide (V factor) and anaerobical y as coccobacil iAmong a-f serotypes, Type b and nontypable strains are the most relevant strains
clinically
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Spread by airborne droplets or by direct contact with secretions or fomites
Colonization with nontypable is a dynamic process and are primarily mucosal
pathogens (EARS, BRONCHUS)
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Hib strains cause systemic disease by invasion and hematogenous spread from
the respiratory tract
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DISEASES BY Hib; Meningitis, Epiglottitis (later age child), Cellulitis, PneumoniaNontypable H. influenzae is the most common bacterial cause of exacerbations
of COPD, Other diseases: otitis media, puerperal sepsis, sinusitis, etc
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Recovery of the organism in culture is most reliable diagnostic methodInitial therapy for meningitis due to Hib should consist of a cephalosporin
Hib conjugate vaccine to all child and chemoprophylaxis with rifampin
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A probable diagnosis of Chancroidcan be made when the following criteria
are met:
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(1) one or more painful genital ulcers;
(2) no evidence of Treponema pallidum
infection;
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(3) a typical clinical presentation for
chancroid;
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(4) a negative test for herpes simplex virus inthe ulcer exudate
Sexually transmitted disease
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characterized by genital ulceration and
inguinal adenitis
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Associated with HIV infectionTreated with single dose of azithromycin or
ceftriaxone
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HACEK organismsGroup of fastidious, slow-growing, gram negative bacteria
whose growth requires an atmosphere of carbon dioxide
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Species belonging to this group include severalHaemophilus species, Aggregatibacter (formerly
Actinobacil us) species, Cardiobacterium hominis, Eikenel a
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corrodens, and Kingel a kingae
HACEK bacteria normally reside in the oral cavity
The clinical course of HACEK endocarditis tends to be
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subacute, particularly with Aggregatibacter or
Cardiobacterium, However, K. kingae endocarditis may
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have a more aggressive presentationLEGIONELLA (IC pathogen)
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Legionellosis refers to the two clinical syndromes caused by bacteria of thegenus Legionella
Pontiac fever (IP- 24-48h) is an acute epidemic, febrile, self-limited il ness that has been
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serological y linked to Legionel a species, whereas
Legionnaires' disease (IP- 2-10d) is the designation for pneumonia caused by these
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speciesSpecies L. pneumophila causes 80?90% of human infections
Natural habitats for L. pneumophila are aquatic bodies
Factors known to enhance colonization include warm temperatures (25?42?C)
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and the presence of scale and sediment; The presence of symbiotic
microorganisms, including algae, ameba, ciliated protozoa, and other water-
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dwelling bacteria, promotes the growth of LegionellaMultiple modes of transmission including aspiration, aerosolization, and direct
instillation into the lungs during respiratory tract manipulations
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Incidence depends on the degree of contamination of the aquatic reservoir,
the immune status of the persons exposed to water from that reservoir, the
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intensity of exposure, and the availability of specialized laboratory testsDif erential diagnosis of atypical pneumonia should be considered
Legionella cultures - best
Legionella urinary antigen test ? highly specific (for L. pneumophila serogroup 1)
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Direct fluorescent antibody (DFA) stainingAntibody testing
Macrolides (especial y azithromycin) and the respiratory quinolones are now the
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antibiotics of choice for 10-14 daysFor critically ill patients, the authors use combination regimens of azithromycin, a
quinolone, and/or rifampin
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Routine environmental culture of hospital water supplies (from cold-water taps,
hotwater taps, the hot-water recirculating line, and water-storage tanks) for
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Legionella is recommended as an approach to the prevention of hospital-acquiredLegionnaires' disease
Copper-silver ionization is a reliable method for eradication
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BORDETELLA (IC pathogen)
Pertussis ("whooping cough"/ "the 100-day cough")is an acute infection of the
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respiratory tract caused by Bordetella pertussisCyclical outbreaks every 3?5 years, can affect people of all ages, However,
Severe morbidity and high mortality rates, are restricted almost entirely to
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infants
B. pertussis infects only humans, B. parapertussis causes a milder illness; and
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rarely by B. holmesii, and B. bronchisepticaMost important virulence factor is pertussis toxin, others are filamentous
hemagglutinin, pertactin, Fimbriae, tracheal cytotoxin, adenylate cyclase toxin,
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dermonecrotic toxin, and LOS
Pathogenesis is unknown after attachment of the organism to the ciliated
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epithelial cells of the nasopharynxIP- 7?10 DAYS
Prolonged coughing illness with clinical manifestations that vary by age
Catarrhal phase, 1-2WKS, (indistinguishable from the common Cold)evolves into the
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paroxysmal phase, 2-4WKS, (the cough becomes more frequent and spasmodic with
repetitive bursts of 5?10 coughs, often within a single expiration, episode may be terminated
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by an audible whoop, which occurs upon rapid inspiration against a closed glottis at the endof a paroxysm), Later into convalescent phase, 4-12WKS, (gradual resolution of coughing
episodes)
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Vomiting with cough is the best predictor of pertussis as the cause of prolonged cough in
adults
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Pneumothorax, severe weight loss, inguinal hernia, rib fracture, carotid artery aneurysm, andcough syncope ? COMPLICATIONS
Laboratory confirmation (Culture of nasopharyngeal secretions ) should be attempted in all
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cases, nowadays being replaced by PCR
Lymphocytosis (an absolute lymphocyte count of >1?10,000/cc ) is common
Pertussis should be suspected when any patient has
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a cough that does not improve within 14 days,
a paroxysmal cough of any duration,
a cough followed by vomiting (adolescents and adults), or
any respiratory symptoms after contact with a laboratory-confirmed case of pertussis
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Purpose of antibiotic therapy for pertussis is to eradicate the infecting bacteria from the
nasopharynx; therapy does not substantially alter the clinical course unless given early in the
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catarrhal phase; Macrolide antibiotics are the drugs of choiceBRUCELLA (undulant fever, IC organism))
Brucellosis is a bacterial zoonosis transmitted directly or indirectly to humans from
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infected animals, predominantly domesticated ruminants and swine
B. melitensis, B. abortus, B. suis, B. canis, B. neotomae, B. ceti, and B.
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pinnipedialisBrucellosis may be acquired by ingestion, inhalation, or mucosal or
percutaneous exposure
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IP- 1 week to several months
Pathogenesis is unknown; The organism is a "stealth" pathogen who avoids
triggering innate immune responses and that permit survival within monocytic
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cells
Brucellosis almost invariably causes fever; dif ers from other fevers,
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(1) Left untreated, the fever of brucel osis shows an undulating pattern that persists forweeks before the commencement of an afebrile period that may be fol owed by
relapse
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(2) The fever of brucel osis is associated with musculoskeletal symptoms and signs in
about one-half of all patients
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Often fits one of three patterns:
febrile illness that resembles typhoid but is less severe;
fever and acute monoarthritis, typically of the hip or knee, in a young
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child;
long-lasting fever, misery, and low-back or hip pain in an older man
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Diagnosis must be based on a history of potential exposure, apresentation consistent with the disease, and supporting laboratory
findings (Culture, PCR, serology)
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Gold standard for the treatment of brucellosis in adults is IM streptomycin
(0.75?1 g daily for 14?21 days) together with doxycycline(100 mg twice
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daily for 6 weeks)Chemoprophylaxis; the administration of rifampin plus doxycycline for 3
weeks after a low-risk exposure (e.g., an unspecified laboratory accident)
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and for 6 weeks after a major exposure to aerosol or injected material
Relapse occurs in up to 30% of poorly compliant patients
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FRANCISELLA
Tularemia is a zoonosis caused by Francisella tularensis
Humans of any age, sex, or race are universally susceptible to this systemic
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infection
It is primarily a disease of wild animals and persists in contaminated
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environments, ectoparasites, and animal carriersHuman infection is incidental and usually results from interaction with biting or
blood-sucking insects, contact with wild or domestic animals, ingestion of
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contaminated water or food, or inhalation of infective aerosols
Characterized by an ulcerative lesion at the site of inoculation, with regional
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lymphadenopathy and lymphadenitisSystemic manifestations, including pneumonia, typhoidal tularemia, meningitis,
and fever without localizing findings may occur
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The diagnosis of tularemia is most frequently confirmed by agglutination testing
Only aminoglycosides, tetracyclines, chloramphenicol, and rifampin are
currently approved (7?10 days)
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YERSINIA
Plague is a systemic zoonosis caused by Yersinia pestis
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It predominantly affects small rodents and is usual y transmitted to humans by anarthropod vector (the flea), Less often, contact with animal tissues or respiratory
droplets
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Patients can present with the bubonic, septicemic, or pneumonic form of the
disease
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Although there is concern among the general public about epidemic spread ofplague by the respiratory route, this is not the usual route of plague transmission
Initial presumptive diagnosis followed by reference laboratory confirmation
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10-day course of antimicrobial therapy is recommendedPostexposure antimicrobial prophylaxis lasting 7 days is recommended following
household, hospital, or other close contact with persons with untreated
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pneumonic plague. (Close contact is defined as contact with a patient at <2 m.)Yersiniosis is a zoonotic infection with an enteropathogenic Yersinia species,
usually Yersinia enterocolitica or Y. pseudotuberculosis
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BARTONELLA
Clinical presentation generally depends on both theinfecting Bartonella
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species and the immune status of the infected individual
Usually a self-limited illness, cat-scratch disease (CSD) has two general clinical
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presentations;Typical CSD, the more common, is characterized by subacute regional
lymphadenopathy;
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atypical CSD is the col ective designation for numerous extranodal manifestations
involving various organs.
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B. henselae is the principal etiologic agent of CSDA history of cat contact, a primary inoculation lesion, and regional
lymphadenopathy are highly suggestive of CSD
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Azithromycin may be given, but limited roleSuppurative nodes should be drained by large-bore needle aspiration and not
by incision and drainage in order to avoid chronic draining tracts
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Thank you