Special Flashcards
Diphtheria epidemiology
Definition: Acute bacterial Infection by cornybac In the stage if elimination . History: 1618- first epidemic in Spain 1884- cultivated by F.Loeffler 1940- toxin vacc in Europe
Etiology Cornybac diphtheria Serology: Gr+ club shape group:4 sub units (GrIMB) Gravis, Intmd, Mitis, Belfanti)
Epidemiology
Loc:developing countries
Age:1-10 y/o
Cycling: autumn/winter before but now not observed
Mortality: previously lethal but no longer
Source & transmissions
anthropomorphism: man 2 man and healthy carriers
Formites: rarely
Mainly inhalation of Droplets 💧by airborne transmissin.
Rarely Contact w/ skin lesions and formites
Contaminated milk
Sick
Morbidity
-countries in low immunisation coveage
Affects kids From 9-20
Demographic structure
Toxic
Non toxic farriers reach 2.5%.
Previous high lethality
Samples for micro tests
- nose, throat typical
- eyes and vagina atypical
Prevention and control
-discover register and examine healthy carriers
Measures againsr it
-timely dg and isolation until 2 megative MBIO results from secretions of the nose and theoat
Contacred ppl are under surveillance for 7 day
Ar risk workers are quarantined
Healthy carriers are isolated till 3-ve results
Imunization schemd
2-3-4 m 26 m
6yr 22 yr
Diphtheria infectious
Clinical features
Depend on strain: toxigenic/ nom toxigenic
And location: Respiratory/ cutaneous
prodrome of half a day to 1 day
Pharyngeal Sx:Sore throat, low fever, tachyK Signs Dirty grey adherent membrane that bleeds on removal Cervical oedema: Bull neck, stridor
Cutaneous
Sx: pain, erythema and numbness
Signs: punched out ulcers w/ gray membrane
Complications Resp: RF complete airway obstruction from detached membrane Paralysed diaphragm CVS: myocarditis and HF CNS: paralysed nerves Toxaemia
Dg( tell ur intern don’t loaf around)
Potassium tellurite: grey colonies
Loeffler coagulated blood serum: rod shaped pleomorphic bacteria w/ methylene blue
Rx
Don’t scrape membrane- obs/bleeding, toxaemia
Immediate diphtheria antitoxin
-only neutralises unbound toxins
-skin/ eye allergy test for horses b4 admin
Soap and water for cutaneous lesions
Drugs: penicillin / erythromycin
Prog
Slow recovery
Rest is essential to prevent myocarditis exacerbation
Prophylaxis: DPT VACCINES
Scarlet fever epidemiology
Definition: acute contagious disease caused by GABHS after URTI of nose, throat, and mouth characterised by generalized toxemia, and a red rash
History
16th century:
first descriBed in med literature as“ROSELLA”
19th century:
renal involvement and STREP assoc discovered by Loeffler
20th century
Loeffler confirmed. Antitoxin made.
Dick test: inject strep wait 24 hr for local rxn
(none= immunity)
Etiology: GABHS
Group
Serology/MB/
Epidemiology Loc: warm temperatures (tropics) Age:10% of 1-10 y/o w/ URTI by GABHS(dip, Cycle:spring and winter Mortality: Decreased since vaccinations
Source & transmission A/Z: anthropomorphism common in 5-15y/o Formites: Droplets 💧 Sputum and pus Contaminated food (milk) Direct contact: wounds, birth canal, toys Contafiois index-35-40%
Characteristics of the disease
Incubation: 12 hrs to 7 weeks
Entry: URT/ per os
Exit: URT
Mech of disease
Pyrogens exotoxins
Streptokinase- brk down of fibrin- excess thrombolysis
M protein virulence factor
-inhibits complement activation & prevents phagocytosis
Carbohydrate antigen A( group A antigen)
Streptolysin O: haemolytic EZ(antigenic)
Streptolysin S: non antigenic
Immunity and receptivity
Immunity is possible in both carrier and infected states but is type specific
Anti epidemiological prophylaxis
Immuno prophylaxis : penicillin/ cephalosporin
No vaccine
Pt management
1)Home isolation 10 days
2)Hospital isolation 10 days w/ penicillin
3)Dispensary examine 20 days after resolution and 3 mo later for possible complication
Correct hygiene and to prevent spread
scarlet fever infectious
clinical features
prodrome: general sx of infection
temperature: 2nd day peak of 40^c. 5-7 day normalises
signs
1)rash
onset: 12-48hrs post fever onset
descripton:
initially sand paper like erythamtous papules , that blanches w/ pressure later becomes boiled and lobulated
location
retroauricular, and neck.
after 24 hrs descends to trunk and flexures of extremities
2)tongue sx day1-2
heavily coated white membrane
sloughs to show red shiny strawberry tongue
3)Pastia lines: 7-10 days after rash resolution
fine desquamation of the skin usually the face
complications: Rheumatic Fever Osteomyelitis
dg:
culture: nose and throat
ASO titres
cbc: leukocytosis w. left shift
rx: NO VACC
penicilline/ 1st gen cephalosporin
epidemiology of meningococcal infection
Definition: group of diseases caused by neisseria meningitidis (meningococcus) causing the syndrome of
1) acute meningitis 2) meningococcemia (sepsis)
History
1805: first descruption in Geneva
greek: meninx=membrane kokkos=berry
Etiology: Neisseria meningitidis Group Serology: 12 types. 6 causes epidemics (AB,C,W,X,Y) ABC =MC Gr -ve bean shape
Epidemiology Loc: A=Africa B=Europe C=USA season:winter-spring Age: 6mo-2yrs and army recruits Cycle environmental resistance: 20^cup 2 5hrs 56^c 5 mins Mortality
Source & transmission
A/Z: anthropomorphism
sick humans (sepsis,meningitis, nasopharyingitis)> carriers. No animal reservoirs
man 2 man by respiratory droplets, throat secretions, kissing
mass gatherings
carried int he throat and hematogenous brain spread
Characteristics of the disease
Incubation: 1-7 days
Entry: nasopharynx
Exit: nasopharynx
Mech of disease
carried assx in nasopharynx or
active infection ID’d by petechial rash d/2 endotoxin release
hematogenous spread causes
1)meningitis
2)Meningiococemia
3)Freidrich waterhause syn= MCC+adrenal insuff
Immunity and receptivity
carriers can develop natural immunity
Anti epidemiological prophylaxis
detect and confirm outbreaks
monitor incidence trends and abiotic resistance profile
Immunoprophylaxis
antibiotics for close contact groups w/ ciprofloxacin and ceftriaxone
3types of vaccination
1) POLYSACCHARIDE: vacc during african outbreaks
innefective b4 TWOyo/ & last 3 yrs
bivalent(A&C) / trivalent(A,C,W)/ tetravalent (A,C,YW)
no herd immunity
2)CONJUGATE vacc; prevention and outbreak
innefective below ONE y/o. 5 year immunity
mono:A mono:C tetra:ACYW
offer herd immunity(protects pop if most are immunised)
3)PROTEIN vaccine: routine immunization and outbreak
against N.meningitidis
Prophylacis with rifampin for contacts
Specifically prophylaxis is the vaccine
infectious diseases meningococcal infection
clinical features” meinigitis , MCC, waterhause freidrich
MENINGITIS
3-5 day incubation and very acute onset
sx: headache, fever, vom, photophobia, hypersensitivity & hyperasthesia
- children: nuchal rigidity, absent, bulging fontanelle, seizures
- adults: DIC, kernig & brudzinski signs
dg:
LP(C.I. IN increased ICP)
-elevated Proteins, WBC mainly NEUT. Decreased Glucose
CT
MCC (acute/ fulminant)
usually follows URTI. early recognition and a.bio rx
complications
cutaneous sx
-petechia and HG, w/ central necrosis in extremities and trunk
-stellate purpura w/ stun metallic gray hue!!
dg:
gram stain of cutaneous biopsy &
KF signs: increased urea & creatinin
non cutaneous sx
- altered mental state
- nuchal rigidity
- irritability
- seizure
WATERHAUSE FREIDHRICH SYNDROM= fulminant mcc
adrenal insuff–>hypotension–>bradyK–>SHOCK
sx: fever, chills, N/V, headache, cyanosis of lower extremities(like infant coarctation of the fucking aorta)
NO MENINGITIS\
Dg
blood culture and cbc;
metabolic disorders:
hypo: glycemia and calcemia . hyperkalemia and acidosis
coag status: increased PT&PTT d/2 DIC
KF signs: increased urea & creatinin
DX
1) aseptic meningitis: LP findings (elevated wbc LYMPH, decreased proteins, normal glucose)
2) Rickets: unlike MCC normal csf and rash begins on wrist
COMPLICATIONS ventriculitis: infants myocarditis skin necrosis requiring amputation permanent neuro sequelae: hydropcephalus, mental retard, cerebral fucking palsy,
rx; ASAP A.BIOTICS
Penicillin G IV. CHLORAMPHENICOL if allergic
Ceftriaxone for CSF penetration
supportive therapy
cerebral oedema; mannitol, dexamethasone, albumin
general: ventilation, O2 therapy, nutrition, hydration is important but overhydration worsens cerebral oedema
epidemiology of pertusis
And parapertussis
Definition: contagious respiratory disease caused by damage of cillia by bordatella pertussis toxins resulting in the characteristic ‘whooping cough’
History
1906- discovery 1932-vaccine1942-DPT vacc
Etiology: bordatella pertusis
Gr-ve
Serology: gravis is worst Mitis is least and Intermedius !!!
Bordatella parapertussis is the same but more mild
Epidemiology:
Loc
Age: 6mo-1yr ; young adults w/o immunization
season
Cycle
Mortality: leading cause of vaccine preventable deaths
Source & transmission
A/Z: anthropomorphism
found in nose and throat
spread by droplets during sneezing and coughing
most contagious in early stage of disease and this period is shortened by abiotics
Characteristics of the disease
Incubation: one week
Entry: URT
Exit: URT
Mech of disease: 4 virulence factors PEFT
1)PERTUSSIS TOXIN: 2 subunits like diptheria except cAMP is the target causing
-histamine sensitization -insulin synth -inhib phagocytosis
2)EXTRACYTOPLASMIC ADENYLATE: weaken host
3)FILLAMENTOUS HEMAGLUTININ`: for cillia binding
4)TRACHEAL CYTOTOXIN: destruction of cilia and epiuthelial cells-> reduced clearance-> WHOOP
Immunity and receptivity
Anti epidemiological prophylaxis
DPT vaccine taken w/in 6 months of life
acellular pertussis vaccines incorporated in immunization schedule
Immuno prophylaxis
combined DPT vaccine in a single injection w/in
Pertisis component is an acellular vaccine
persussis infectious
pertussis is a 6wk infection divided into 3 stages lasting 1-2wks each
1) catarrhal(URTI)
fever plus
nose:rhinitis, sneezing& nasal conjestion
eyes: conjunctival suffision(redness w/o exudate) & tearing
2)paroxysmal(cough develops)
intense coughing paroxysms for several mins w/ WHOOP
posttussive vomitting and redness of the face
cough like the cat meme(tongue, eyes, engorged veins)
3)convalescence
chronic cough for weeks and pt is contagious
dg of pertussis
B.pertussis culture: nasopharyngeal aspiration in 1st 2 wks of cough
PCR: specimen taken up to 3wks after cough develops
RX: supportive
rest& recovery
drugs: MACROLIDES for age one and above(erythromycin, clarithromycin, azithromycin)
prophylaxis: DTaP vaccine & Tdap vaccine: 7+y/o
epidemiology of salmonella
Definition: bacterial infection by any species of salmonalla with varying severity
History
19th c: defined by pathological(anatomical) changes
1880 Eberth observed in spleen sections
1881 R. Koch – isolated in media
1896: serodiagnosis was discovered from serum of immunized animals
Etiology determines pres
1) enteric fever
- S.typhi = typhoid fever
- S.paratyphi A,B,C = paratyphoid fever
2) enterocollitis
- S.typhimurioum
- S. enteritidis
3) bacteremia & focal lesion
- Salmonella choleraesuis
Serology: over 3000!!! Gr-ve bacilli O-ag - thermostability H-ag flagella for motility typhoidal: Vi-ag- virulence d/2 capsulation capsulated nontyphoidal: non caps O-ag & H-ag allows motility
Epidemiology
Loc
typhoidal: :Asia, Africa, parts of South America and Oceania
Age:0-1 most affected season: -rainy season in tropical climates. -summer in northern hemisphere Cycle: typhoidal-human is obligate enterococcal: cattle, poultry, pigs, and human excrement. doesn't replicate in env survive in a weeks in water, years in soil Mortality
Source & transmission A/Z: typhoidal: anthropomorphism: enterocollitis: zoonosis fecal-oral sexual contact in homosex rare carriers and sick shed bac in feces assx carriers: recover but still shed especially if gallstones are present as residual bacteria reamins in gallbladder (cholecystectomy resolves this)
Characteristics of the disease Incubation typhoidal: water: up to 90days meat/fruit: 3 wks non t gastroenteritis: 12hrs-3 days enteric fever: 10-14 days Entry: Exit: feces
Mech of disease: release of endotoxin causing GI SX
mechanisms:
1) adherance to GI &
2) invasion of macrophages and replication w/in the SALMONELLA CONTAINING VACUOLE & immonumodulation by Lipid A
3) dissemination & survival in w/in reticuloendothelial system
1) adhesion risk increases during decreased barrier defences
- low gastric acid increases risk(PPI, atrophic gastritis)
- pancreatic ez insuff(pancreatitis, CF)
- reduced bile salts (cholestasis/lithiasis)
2) invasion risk increases during reduced cell mediated immunity (HIV, Malig, immunosuppressants
Immunity and receptivity
typhoidal immunity is fairly stable w/ possibility of relapsed/2 loss of agens by abiotic activity
Anti epidemiological prophylaxis
-hospitalization of patients, disinfection of the sources, and identification
treatment of carriers
Washing of hands before meals and after using the toilet is necessary
2)non typhoid
improve health education, water and sanitation
travellers advice avoid risky food and drink! avoid ice unless its from bottled water eat food that is still hot and steaming avoid raw fruit that cant be peeled peel fruit and dont eat peelings
Immuno prophylaxis
typhoidal
-typhoid vaccine (monovaccine),
-typhoid and paratyphoid B vaccine (divaccine).
nontyphoid
no vaccine.
abiotic rx w/ chloramphenicol , ampicillin although MDR strains are emerging needing rx w/ flouroquinolones
Measures against disease
Isolation and hospitalisarion until 1 negarive result from fecal sample
Risk group isolated extra 15 days with 1 test every 5 days w/ 3 negative resukts.
If one is positive extra 15 days
Measures against contacts
MBIO test of contacts. No work till result of tesr. If positive no work dor 15 days till 1 negarive reshlr
Agaibst envirknme t
Disinfection, disinsection.
No effective vaccine d/2 mamy seritypes
salmonella infectious
clinical manifestations
typhoid fever
-acute general infection of the reticuloendothelial
system, intestinal lymphoid tissue, and the gall bladder). —-Sx are often non-specific,
clinically the same as other febrile illnesses (causes frequent misdiagnosis).
non typhoidal gastroenteritis sx
- mucopurulent diarrhoea w/o blood 6-48hrs after ingestion
- can mimic S.I. diarrhoea w/ small vol or L.I diarrhoea w. arge vol & tenesmus or present as pseudoappendicitis (LRQ pain
dg
culture: stool/blood
echocardiography in positive blood culture and high fever
complication typhoid fever intestinal haemorrhage, intestinal perforation cholecystitis. bacteremia(esp in immunocomp) --> endocarditis, -->osteomyelitis -->cns infection in NEONATES -->septic arthtitis in HbSS -->septic shock nontyphoid reiter's syndrome
rx
of typhoid fever
First-line: chloramphenicol, ampicillin, or cotrimoxazole.
d2 multidrug
resistant in strains in the alternatives are fluoroquinolones,
third-generation cephalosporins, and azithromycin.
epidemiology of shigellosis
aka bacterial dysentry (inflammatory disease of the intestine, especially of the colon, which always results in severe diarrhea and abdominal pains)
Definition: infectious disease of the intestines caused by infection w/ shigella fam of bacteria presenting as dysentry w/ bloody diarrhoea
History
1897. discovered by Japanese microbiologist Dr. Kiyoshi Shiga
Etiology: shigella family -Short rods - Non-encapsulated - Non-motile - Non-spore former -Gram-negative aerobic/facultative anaerobes
Serology: 4 serogroups
- Shigella dysenteriae group A
- Shigella flexneri- group B
- Shigella boydii -group C
- Shigella sonnei -group D
pathogenic determinants -O antigen: survive the host defenses - Epidemiology Loc; premon developing countries S.sonnei predomin even in high income countries. Food products S.flexneri- Africa and Asia. Water transmission Age: mainly children under 6 season:season Cycle Mortality: 1999 a million deaths dropped to 5000 in 2013 now0.003% Contagious index is 30% Source & transmission A/Z: anthropomorphism sick and carriers d/2 poor sanitation and polluted water -fecal oral -man 2 man -flies -water -formites
Characteristics of the disease Incubation:1-7 days (longer in water) Entry:oral Exit: feces
Mech of disease
cytotoxic shiga toxin–> bloody mucus discharge
enterotoxin–> watery stool
neurotoxin
uneven intestinal mucosal penetration
invades enterocytes &multiply, then nvades neighbouring cells
shiga toxin disrupts protein synthesis leading to cellular death.
cell necrosis and phagocytosis response by the host causes bloody
discharge of mucus and pus and shallow ulcers characteristic of the
disease.
Immunity and receptivity
serotype spicific
SIgA immunoglobulins
limited d/2 various serotypes
Anti epidemiological prophylaxis
health education
correction of contaminated water
Avoid sexual contact w/ ppl w/ diarrhoea now or recently(2weeks)
Immuno prophylaxis no vaccine antibiotics frequent handwashing food safety
infectious of shigella
clinical
high fever and charac sx of lower GI: abdominal cramps,
intially watery then bloody, mucoid, diarrhea.
tenesmus(8-10-100x/day)
small vol- dehyd unlikely
(S.I. has large vol)
comp of intestine S.dysenteriae(worst pres) -toxic megacolon -perforation systemic comp -bacteremia -seizures in children -encephalopathy -HUSHAT-life threatening
dg
CBC:Leukocytosis, Neu↑, shift to the left, ESR↑,
Lab: Hypoelektrolytemia: Na ↓, K↓, Cl↓, metabolic
acidosis
def dg: stool culture on agar
dx:
bac diarrhoea: salmonella, C.jejuni,
parasitic diarrhoea: entemeba hystoliticatious diarhhoea: IBD
non infec
rx supportive: general gastroenteritis support -correct fluid/ electrolyte bal -nutrition antimotility drugs C.I(prolog fever)
abiotic therapy
ceftriaxone in children
epidemiology of cholera
Definition: acute infection of S.I by vibrio cholera characterised by watery diarrhoea
History
1817: first cholera pandemic in Jessore, India, from contaminated rice.
1854, the worst single year of
British physician John Snow ID cause was d/2 infected well pump
Italian microbiologist Filippo Pacini I.D’d the cholera bacterium—naming it cholerigenic vibrios
1883 kock grows v.cholera and confirms its presence in intestines
2017 outbreak in yemen and somalia was the largest epidemic of recent times
Etiology: vibrio cholerae
Serology: hundreds but
serogroups O1 and O139 are the only two strains causing epidemics d/2 toxins
Epidemiology
Loc:Asia (esp India), Middle East, Africa, South and Central America,
Gulf Coast of USA.
Age; all ages equally susceptible
season: warm seasons
Cycle
Mortality: 3-5 million cases and 100,000-130,000 deaths per year.
Source & transmission
A/Z: anthropomorphism
fecal oral by contact w/ infected water or feces
Characteristics of the disease
Incubation; -12 hrs- 5 days
Entry: oral
Exit: feces
Mech of disease
5 beta subunits surround A subunit
B subiunit grants acces into small intestine epithelial cells by GM1 channel
A subunit actives cAMP–> activates chloride transport protien–> influx of Cl- & H20 into cell. IC capacity becomes full and releases excess water in stool as watery diarrhoea
immunity
People living in endemic areas gradually acquire a natural immunity.
Anti epidemiological prophylaxis
-human excrement must be correctly disposed of
-water supplies
purified.
drinking water should be boiled or chlorinated
veg and fish cooked thoroughly.
Immuno prophylaxis
3 types of ORAL vacc w/ 2 doses .
o Vaxchora. live-attenuated, single-dose monovalent oral vaccine. FDA approved
o dukoral, shachol. Two dead whole-cell oral vaccine
booster doses after 2 yr for people with ongoing risk of cholera.
cholera infectious diseases
sx: rice water stool!!!
Abrupt, painless, watery diarrhea & vomiting
Significant nausea is
typically absent
Stool loss in adults may exceed 1 L/h but is usually much less.
Often, stools consist of
white liquid void of fecal material (rice-water stool).
comp
dg
- Stool culture and serotyping
- Rapid dipstick testing for cholera
- Serological tests
rx
1.Fluid replacement
- Doxycycline, azithromycin, furazolidone, results of susceptibility testing
epidemiology of
Definition:
History
Etiology
Serology
Epidemiology Loc Age season Cycle Mortality
Source & transmission
A/Z
Characteristics of the disease
Incubation
Entry
Exit
Mech of disease
Immunity and receptivity
Anti epidemiological prophylaxis
Immuno prophylaxis
