Special Flashcards

(39 cards)

1
Q

Diphtheria epidemiology

A
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

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2
Q

Diphtheria infectious

A

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

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3
Q

Scarlet fever epidemiology

A

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

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4
Q

scarlet fever infectious

A

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

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5
Q

epidemiology of meningococcal infection

A

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

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6
Q

infectious diseases meningococcal infection

A

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

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7
Q

epidemiology of pertusis

And parapertussis

A

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

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8
Q

persussis infectious

A

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

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9
Q

epidemiology of salmonella

A

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

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10
Q

salmonella infectious

A

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.

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11
Q

epidemiology of shigellosis
aka bacterial dysentry (inflammatory disease of the intestine, especially of the colon, which always results in severe diarrhea and abdominal pains)

A

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
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12
Q

infectious of shigella

A

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

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13
Q

epidemiology of cholera

A

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.

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14
Q

cholera infectious diseases

A

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

  1. Stool culture and serotyping
  2. Rapid dipstick testing for cholera
  3. Serological tests

rx
1.Fluid replacement

  1. Doxycycline, azithromycin, furazolidone, results of susceptibility testing
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15
Q

epidemiology of

A

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

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16
Q

infections

17
Q

epidemiology of

A

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

18
Q

epidemiology of poiliomyelitis

A

Definition:

Candidate of elimination. 2018 only cases in afghanistand and pakistan
Eradicated in europe sonce 2002. Bulgaria 2001

History
-WPV 2 virus has been successfully interrupted globally and was last reported
in 1999.

Etiology
Poliovirus is an RNA virus in the family Picornaviridae,
genus enterovirus,
-Poliovirus type 1 causes most paralytic manifestations of poliomyelitis.

Serology
three serotypes: 1,2 and 3.

Epidemiology
Loc;
-endemic in Afghanistan, Nigeria, and Pakistan.
Age:
-Children under five are at highest risk.
season
Cycle:
-Soil, sewage and
infected water have been shown to harbour the virus.
Mortality

Source & transmission
A/Z: anthro
human only known resevoir
-via droplets or aerosols from the throat and by
faecal contamination of hands, utensils, food and water.

Characteristics of the disease
Incubation
-7-10 days is when polio is most infective. (range 4-35 days)

Entry:oral
Exit: fecal/oral

Mech of disease
–The virus replicates in the gastrointestinal tract following oral ingestion →
enters the bloodstream → potential invasion of the grey matter of the spinal
cord (particularly the anterior horn cells)

Immunity and receptivity 
-Infection or
immunisation with one serotype does not induce immunity against the other
two serotypes.
Anti epidemiological prophylaxis 
Vaccine is IM

Immuno prophylaxis
-Provision of clean water, improved hygienic practices and sanitation are
important for reducing the risk of transmission in endemic countries.

19
Q

infectious diseases of poliomyelitis

A

classification

  • Abortive poliomyelitis- 4-8%
  • Nonparalytic poliomyelitis-
  • Paralytic poliomyelitis
clinical features 
95% of infections are asyx
1)abortive
fever,
headache, vomiting, diarrhea, constipation, and sore throat lasting 2-3 days.

2)non paralytic
-abortive sx
-meningeal
irritation: neck stiffness, photophobia, headache. -Muscles spasms
-absence of frank paralysis.
3)paralytic; assymetric flaccid
-Spinal
affects muscles innervated by the spinal nerves, and -bulbar
weakness of the muscles supplied by the cranial nerves and of the
Respiratory and Vasomotor centers

dg
PCR: throat stool, LP: lymphocytes) and a mildly elevated protein level. Detection of virus in the CSF is
diagnostic of paralytic polio, but rarely occurs

rx
acute phase of paralytic poliomyelitis:
Hospitalization & Strict bed rest.

respiratory weakness or paralysis-intensive care.

recovery: Intensive physiotherapy-
some motor function with paralysis.

prevention
parental vaccination of inactive polio

20
Q

epidemiology of measles

A

definition: infectious viral disease causing fever and a red rash, typically occurring in childhood

History
first live attenuated vaccine was licensed for use
in the 1960s (Edmonston B strain).

9 years later In Bulgaria-1969

Etiology
-Paramyxovirus (single stranded RNA)

Belongs to genus Morbilivirus, family Paramyxoviridae
Serology

Epidemiology 
Loc: global
Age; young children
season:
-tropical: dry season
-temperate: winter
Cycle
Mortality/ burden
-since the
study of Andrew Wakefield who linked MMR vaccine to autism  more
parents don’t want to vaccinate their children. In Bulgaria there was an
epidemy in 2009 to 2010

Source & transmission
A/Z: anthropomorphic
Person to person via large respiratory droplets.
Most infections from prodrome-first 3–4 days of rash.

Characteristics of the disease 
Incubation: 
-till prodrome10-12 days  
-till rash 14 days
Entry
Exit

Mech of disease
-primary infecrion of
nasopharynx.
-2-3days replication in the
respiratory epithelium and regional lymph nodes leads to a PRIMARY VIREMIA
-allows infection of reticuloendothelial system.
-more replication in
reticuloendothelial sites, causes a SECOND VIREMIA 5–7 days after initial
infection.
2nd viremia allows infection of the respiratory
tract and other organs.
-measles sheds from nasopharyx during
prodrome until 3–4 days after rash

Immunity and receptivity

Anti epidemiological prophylaxis

Immuno prophylaxis
- Live vaccine combo MMR  – 2 doses
  lifelong immunity
FIRST dose 
MMR at 12-15 months
-b4 12 mo is invalid 
req revaccination

SECOND dose of MMR at 4-6 years

  • atleast 4wks after 1st
  • gives measles immunity if first dose failed

C.I.
-Anaphylactic reaction to neomycin,
-immunosuppression, moderate/severe
acute illness, family history of seizures of any etiology

21
Q

infectious of measles

A
clinical features
incubates for 12 days
12th prodrome
lasts 2-4 days
sudden fever
catarrhal phase
URT sx
Kolplik spots
pathognomic 
sand grains 
rash phase
cephalocaudal spread
maculopap BRICK RED CONFLUENT
fades after 4 days
1-2 days pts v. ill
fades after 3-4 days

complications
d/2 temp immunoDEF
cause of death

respiratory
croup, otitis media
adults-pneum

CNS
• encephalitis
• meningoencephalitis
• Subacute sclerosing panencephalitis (SSPE) is rare complication in children under 2
degenerative CNS
disease, after contracting measles occurs 7 years later.

dg
clinical: Exposure + cough, conjunctivitis, Koplik’s spots, confluent maculopapular rash, vacc history & recent travel

LAB - 
Lc↓, ALAT↑
• serology ELISA IgM (+)
• viral isolation important for molecular epidemiological surveillance - define
geographic origin
dx
Kawasaki disease
• Scarlet fever
• Infectious mononucleosis
• Toxoplasmosis
• Drug eruption
• Mycoplasma pneumoniae infection

rx
hospitalization and isolation:
-immuno comp- whole duration of illness

supportive:
- VitA, VitC,

complic: AB (bacterial infection), corticosteroids (obstruction)

prevention 
MMR vacc
post exposure proph
-Vaccine within 3 days,
-immunocompromised patients should received IG 0.5ml.kg IM
within 6 days of exposure.
22
Q

epidemiology of mumps

A

Definition: (Epidemic Parotitis) is an acute, generally a mild childhood
disease, primarily affecting the salivary glands.

History

Etiology
-Virus parotitidis (mumps virus)
-Paramyxoviridae family 
-genus Rubulavirus
-room temperature
can survive 4-6 days –
disinfection!

Serology
-one serotype of the virus and in the
patient, it can be found in most body fluids including CSF, saliva, urine and blood.

Epidemiology
Loc
Age:
-affect school-aged children. It is unusual to see mumps in infants,
because of the mother’s AB remains protective for the first year

season: Peaks predominantly in late winter and spring, but the disease has been

reported throughout the year.
Cycle
Mortality

Source & transmission
A/Z: anthrop
No carrier state!
infected assx/ prordrome only

droplet in air or saliva

Characteristics of the disease 
Incubation: 
12 to 25 days
Entry
Exit

Mech of disease
-Replication in nasopharynx and regional lymph nodes
-After 12 to 25 days a viremia occurs, lasting 3 to 5 days.
-During the viremia, virus spreads to multiple tissues:
MENINGES and glands such as the PAROTID, pancreas, testes, and ovaries.
-Inflammation in infected tissues leads to characteristic symptoms of
parotitis and aseptic meningitis.

Immunity and receptivity
-[Natural infection leads to lifelong protection]

Anti epidemiological prophylaxis
- vaccination

Immuno prophylaxis
- Live vaccine combo MMR  – 2 doses
  lifelong immunity
FIRST dose 
MMR at 12-15 months
-b4 12 mo is invalid 
req revaccination

SECOND dose of MMR at 4-6 years

  • atleast 4wks after 1st
  • gives measles immunity if first dose failed

C.I.
-Anaphylactic reaction to neomycin,
-immunosuppression, moderate/severe
acute illness, family history of seizures of any etiology

23
Q

infectious of mumps

A

clinical
incubation :12 to 25 days (2-3wks)

prodromal: 1-2 days before specific sx
-nonspecific and include mild fever, anorexia,
malaise, myalgia and swelling of Stenson’s duct.

classical mumps sx

1) Fever
2) Parotitis : MC
- Painful parotid swelling persists for 7 - 10 days
- unilateral or bilateral.
- discomfort while chewing or speaking.
2) Aseptic meningitis
- usually mild. -m>f adults>kids
- 50% asyxx
- 50% stiff neck and headache which resolves in 10 days unless enceph
4) Deafness : less common after vacc
- unilateral.
- transient or permanent.

rare complications
nephritis, arthralgia, hepatitis and arthritis.

dg
-clinical
-viral isolation by 
RT-PCR or by serology.
-ELISA:IgM rise during the prodromal phase and peak at about seven days.rx

rx
MMR vaccine w/ 2 doses seperated by 4 weeks for children over 1 years old

24
Q

epidemiology of rubella

A

Definition: German measles or three-day measles, is an infection caused by the rubella virus. This disease is often mild

History

Etiology
Rubella virus family Togaviridae
Serology:

Epidemiology
Loc
Age: children and young adults.
season: late winter/ spring
Cycle
Mortality/ burden:leading vaccine-preventable cause of birth defects.
Rubella infection in pregnant women may cause foetal death or
congenital defects known as congenital rubella syndrome (CRS).

Source & transmission
A/Z: anthro
-transmitted by persons with subclinical or asymptomatic
-vertical transmission

Characteristics of the disease
Incubation; Average of 18days
Entry
Exit

Mech of disease
-Respiratory transmission of virus
-Replication in nasopharynx and regional lymph nodes
-Average of 18days 5 to 7 days after exposure with spread throughout body
-Transplacental infection of foetus during viremia affecting all organs and causing
death/ prematurity
-Severity of damage to fetus depends on gestational age.
85% of infants affected if infected during first trimester

Immunity and receptivity
-most contagious when the
rash first appears, -virus may be shed from 7 days before /after rash onset.

Anti epidemiological prophylaxis
MMR VACC

Immuno prophylaxis
- Live vaccine combo MMR  – 2 doses
  lifelong immunity
FIRST dose 
MMR at 12-15 months
-b4 12 mo is invalid 
req revaccination

SECOND dose of MMR at 4-6 years

  • atleast 4wks after 1st
  • gives measles immunity if first dose failed

C.I.
-Anaphylactic reaction to neomycin,
-immunosuppression, moderate/severe
acute illness, family history of seizures of any etiology

Meausres against contaxt ppl

  • medical surveillance for 30 days
  • kindergarten 20 days, nom immunised ppl not allowed contact

Pregnancy
-serological testing to check infextious starus
-1st test less than 1:32 requires immunigloblin
Above this have immunity
-2nd tesr is 4x higher then the woman has recent infections and abortion is reccomended
-sick leave given for kindergarten workers for the test

Measutes against enc

  • unstabe im env so not ness
  • immunisation done for 13 months along witj measles and mumps
25
infectious of rubella
clinical of rubella 50% of ppl are subclinical incubation 12-23days/ (2-3wks) prodrome: usually none rare: conjunctivitis, runny nose rash: 1st sx spreads for 1 day, lasts about 3 days, maculopapular: DISCRETE (not confluent like measles) hemorrhagic exanthema 20% •Lymphadenopathy- appears a week before the rash, last several weeks after it loc: postauricular, posterior cervical, suboccipital(theodor sign) dg difficult to dg rubella because: 1)clinical diagnosis unreliable 2)LAB -unremarkable, leukopenia and atypical lymphocytes. CRS indicates- viral culture, (PCR) serology (ELISA) - IgM in single sample is often (false (+)! - IgG seroconvertion: acute and convalescent ``` ddx: PETS 5 roses Enteroviruses, Parvovirus B19 (erythema infectiosum), Toxoplasmosis, Scarlet fever, Modified measles, Roseola, Fifth disease ``` ``` CONGENITAL RUBELLA SYNDROME transient birth sx A: Autism, B: Bony abnormalities, Behavioral disorders, C: Cloudy cornea, Congenital heart disease (pulmonic stenosis), Cryptorchidism, CP D: degenerative brain diusease G:Glaucoma, H:Hepatitis, Hepatosplenomegaly, I: ITP J: JAUNDICE L: Lymphadenopathy, Low birth weight, ``` dg maternal blood sample ASAP and test for rubella antibodies if: 1)rubella specfic ab IgG =maternal immunity CRS-ve 2)no anit rubella igG in blood: serum test in 2 wks -negative test result in both specimens indicates that infection has not occurred. Advice for vaccination -seroconversion: positive test result (IgM) in the second and not the first indicates recent infection – counseling for termination of pregnancy rx •Isolation: 7 days after onset of rash, congenital: till 1 y/o Treatment: supportive Prevention: immunization MMR vaccine
26
Epidemiology of Q-rickettsiosis /
Definition:Q fever History Etiology - Coxiella burnetii - Obligate intracellular parasite. Stable and resistant. Killed by pasteurisation Serology -Two antigenic phases: Phase 1- virulent. Phase 2: less pathogenic ``` epidemiology Loc Worldwide, except New Zealand Age: vets, meat processing plant workers, dairy workers, livestock farmers season Cycle: -sheep, goats and cattle-can grow in large numbers in the female’s uterus and udder. dust humans Mortality ``` ``` Source & transmission A/Z: zoonotic contaminated milk / contact with foetus, placenta or fluids from when an animal gives birth. ihnalation of dust ``` ``` Characteristics of the disease Incubation: 2-6 weeks Entry Exit ``` Mech of disease -C. burnetii infects the respiratory tract. burnetti can survive and grow within acidic phagosome because of its sodium ion/proton exchangers. makes curing chronic Q fever with antibiotics difficult. --------------Pulmonary infection causes infiltration by mononuclear cells--> focal necrosis and haemorrhage. spreads to the liver, causing GRANULOMA . -chronic endocarditis occurs in susceptible pts Immunity and receptivity Anti epidemiological prophylaxis - Good hygiene practices in premises dealing with animals - pasteurisation of milk and milk products Immuno prophylaxis - Q-Vax, a whole-cell, inactivated vaccine. - single dose intradermal vaccination is composed of killed C. burnetti - life long protection  blood test for existing immunity to avoid severe local reaction.
27
infectious of q fever
sx abrupt flu-like illness w/ dry cough. (10% of cases), a maculopapular rash appears. complications - ARDS - hepatitis with elevated transaminases, but minimal elevations in bilirubin; - myocarditis - pericarditis; - chronic endocarditis (negative echo early in the disease, high mortality) - meningitis; DG =cultures are not performed because of the danger to lab personnel. =PCR -Elevated IgG and IgM antibody indicate acute disease. -Elevated IgG and IgA antibody titres against phase I antigens are diagnostic of chronic Q fever. ``` RX Abiotics less effective self-limiting, lasting 2 weeks. !!Oral or intravenous doxycycline is the treatment of choice, and fluoroquinolones are considered a reasonable alternative.!! ``` longer therapy needed in chronic endocarditis
28
Epidemiology of Mediterranean Spotted Fever
Definition: History Etiology Rickettsia. Conorii through the bite of the brown dog tick Rhipicephalus. Sanguineus. ``` Epidemiology Loc; Mediterranean area (Greece, Turkey, Romania and Bulgaria,) and southern Europe (italy, spain) Age/ risk group dog owners season Cycle Mortality ``` Source & transmission A/Z Characteristics of the disease Incubation Entry: skin, conjunctiva. w. charac tache noire Exit Mech of disease tick borne Immunity and receptivity Anti epidemiological prophylaxis - avoid close contact w/ animal vectors in endemic areas - Protective clothing w/ permethrin - freq Topical repellents on exposed skin; - daily self checks immuno prophylaxis -no vacc
29
infectious for Mediterranean Spotted Fever or Boutonneuse Fever
``` clinical triad of MSF Fever: Rash (exanthema) lower legs, 2-6 days after fever Tache noire ``` DG - clinical feature - history: tick bite, which is typically tick bite is painless and can go unnoticed - contact with a dog; - recent travel to an endemic area. serologic test classic Weil-Felix test using biopsy of primary lesion ``` rx self limiting (2weeks) abiotics speed up recovery and reduce fever -Tetracyclines, ```
30
Epidemiology of Congo-Crimean Fever
Etiology: Nairovirus – tick borne virus (Bunyaviridae fam) Ixodid (hard) ticks, especially those of the genus, Hyalomma, are both a reservoir and a vector for the CCHF virus. cattle, goats, sheep and hares, serve as amplifying hosts Serology Epidemiology Loc: endemic in Africa, the Balkans, the Middle East and Asia, countries south of the 50th parallel north.( south of a a line thats 50 degrees north of the equator) Age/ risk group slaughterhouse workers & animal herders in endemic areas season Cycle Mortality Source & transmission A/Z: zoo contact with infected ticks or animal blood. anthro: contact w/ infected blood Characteristics of the disease Incubation: 5-6 although 13 max has been seen Mech of disease Immunity and receptivity ``` Anti epidemiological prophylaxis risk groups should -use Insect repellants containing DEET ( diethyl-m-toluamide) -avoid blood contact -raise awareness ``` Immuno prophylaxis -NO VACC health care prophylaxis -basic hand hygiene, use of personal protective equipment, safe injection practices and safe burial practices.
31
infectious for CCHF
clinical features sudden onset of consitutional sx typical sx for CCHF -Red eyes, a flushed face, a red throat, and petechiae (red spots) on the palate are common. 4th day-2wks progressive hemorrhagic sx -severe bruising, severe nosebleeds, and uncontrolled bleeding at injection sites dg: LAB RT-PCR ELISA culture: viral isolation rx: supportive - correct fluid electrolytes - correct metabolic abnormalities - rx of any 2ndary infec curative a.viral RIBAVIRIN oral/I.V
32
Epidemiology of Lyme Disease
``` Etiology Borrelia burgdorferi, anaerobic, facultative intracellular spirochete bac Serology ``` ``` Epidemiology Loc Age season Cycle Mortality ``` Source & transmission A/Z: zoonotic through a bite from an infected tick, mainly a nymph or an adult. longer blood meal= increased risk of infection Characteristics of the disease Incubation: 3-30 days. Mech of disease skin Inoculation after meal--> ERYTHEMA MARGINATUM d/2 replication -->invade vessels & spread haematogenously to other organs (skin, CNS and joints)--->stim immune response==>specific IgM ab’s peak at 3rd -6th week after onset immunity and receptivity Anti epidemiological prophylaxis - early removal of attached ticks w/ tweezers as closely as possible to the skin, pulling gently upwards and trying not to break off the mouth parts. -wearing protective clothing, like long trousers and long-sleeved shirts, and using tick repellents. -regular skin checks of skin-folds e.g. groins, armpits, under breasts, waistband area, backs of knees—as ticks seek out more humid areas for attachment. Immuno prophylaxis NO VACCINE for lyme disease --Permethrin-impregnated clothing can be used by people who have frequent heavy exposure to ticks, such as forestry workers or military personnel on exercise.
33
infectious of lyme disease
early sx of lyme diseaseare flu like 3 stages of lyme disease sx Early LOC Lyme: Flu-like symptoms and typical 5 centimeters rash w/ Erythema migrans BULLS'EYE or uniform round red appearance Early DISS Lyme: Flu-like symptoms & CNS sx: pain, weakness or numbness in the arms and legs, vision changes & Bell's palsy & CVS sx: palpitations and chest pain LATE DISS Lyme: weeks, months, or years after the tick bite: arthritis, severe fatigue neck stiffness and headaches, vertigo, sleep disturbances, and mental confusion. dg of lyme - history of tick exposure - clinical sx - serolgy only in pts w/ specific signs and sx of lyme rx of lyme early: doxycylcine 10 days disseminated early and late: ceftriaxone 21 days
34
epidemiology of HIV/AIDS
Definition: presence of one of 25 conditions indicative of severe immunosuppression in HIV + person OR HIV infection in an individual with a CD4+ cell count of less than 200 cells per cubic mm of blood. History Etiology Lymphotrophic lentivirus  retroviridae fam Consists of the two species HIV-1 and HIV-2  serology Epidemiology Loc:  HIV-1: most common species worldwide   HIV-2: restricted almost completely to West Africa ``` Age/ RF -unprotected sex (oral,vaginal,anal) -other STI syphilis, herpes, chlamydia, gonorrhoea, and bacterial vaginosis; -I.V drug use -unsafe bloodtransfusion/ tissue transplant -needlestick injury ``` season Cycle Mortality Source & transmission A/Z: anthro Sexual: 80% of infections worldwide -semen/ vag secretions Parenteral: Needle sharing, needlestick injuries, blood transfusions. Vertical: During childbirth or through breastfeeding after birth CANNOT ordinary day-to-day contact such as kissing, hugging, shaking hands, or sharing personal objects, food or water Characteristics of the disease Incubation: approx 10 years Mech of disease 1. Acute HIV Infection: HIV multiplies rapidly and spreads throughout the body. virus destroys fighting CD4 T cells of the immune system. HIV in the blood is very high, which greatly increases the risk of HIV transmission. 2. Chronic HIV Infection HIV continues to multiply but at very low levels. pts are asxx still spread HIV to others. AIDS in 10 years or so w/o rx 3. AIDS HIV has severely damaged the immune system Opportunistic infections & infection-related cancers increase in severity/freq-death in 3years w/o rx Immunity and receptivity increased adhesion of HIV to anal epithelium Anti epidemiological prophylaxis practice safe sex -condoms, reduced promiscuity avoid needle sharing PROPHYLAXIS AFTER HIV EXPOSURE indicated in 1)Injury with HIV-contam needles 2)Contamination of open wounds or mucous membranes with HIV- contaminated fluid 3)Unprotected sexual activity with a known or potentially HIV-infected person procedure initate ASAP(1-2hrs) Drugs: A three-drug regimen 1)nucleoside reverse transcriptor inhibitor(Tenofovir) 2)nucleotide reverse transcriptase inhibitor (emtricitabine) 3)integrase inhibitor: (dolutegravir/raltegravir) VACCINATIONS IN HIV PTS -reduced efficacy (d/2 impaired immune function) general immunization precautions in HIV - Inactivated vaccines are safe - Live vaccines CI exceptions to immunization schedule -inactivated polio isntead of attentuated -live-attenuated  influenza, varicella zoster, and MMR vaccines should not be given in AIDS determined by (CD4 count below 200 cells/μl  or CD4 is only 15% in patients ≤ 5 years or if AIDS-defining conditions are present. T NEEDLE STICK INJURY RX  Let the wound bleed  Rinse/flush with water and soap and/or antiseptic agent  Immediately seek medical attention
35
infectious of aids
3 stages ``` acute sx -Fever over 38°C, for 2 months -diarrhoea over 1 months -Wasting syndrome -Decreased body weight (over 10%) -Persistent Generalised Lymphadenopathy over 2 months at ≥2 extra inguinal sites ``` chronic asx AIDS Opportunistic infections -Pneumocystis pneumonia, -Tuberculosis, -Toxoplasmosis, -Candidiasis Neoplasms -----------Kaposi, - Hodgkin’s Lymphoma - Non-Hodgkin’s Lymphoma Neurological disorders dg 2 positive ELISA tests • CD4 number(below 200) or percentage(below 15%) • Virological markers: PCR (positive, at 400 copy/ml), Viral Load, HIV resistance tests ``` Lab pancytopenia pleiocytosis low albumin elevated acute phase proteins & liver ez ``` rx There is currently no cure or effective HIV vaccine. triple drug Highly Active Anti Retroviral Therapy 2NRTI plus 1 proteiase/integrase inhibitor
36
Epi of varicella
Caused by varicella zoster. Ins human herpes virus 3 Rna virus and instable In environmental Contagious in last 2-3 days of the incubation period. Once scabs form no more ciruses are released MOT - airborne. Carried by longer diseases than airborne biruses - person 2 person contact from rash - vertical from preg women to embryo Measures against disease - isolation at home till scabs form - hospitalised when: Meausred afainst contexted person -children in under 7contact monitured fot 21 years -kindergarten pol obvs for 21 years. Disinfection not necc
37
Influenzas epidejology
Etionis influenza viris from 3 types. ABC 2 antigens(H) hemagluttinin and M High mutabiloty causing epidemic strains Unsrable in environment Soread by secretions bt diseased and assyx pol Airborne aMot Contagious index is 90-100% Affects children and old sdults Immunity is tyoe soecific for one year Vaccines for risk grouos Measures afainst disease - isolation for 3 days - hospital for epidemiology indications - symptomatic drugs and immunomodulators Cleanin of the environment Under the control if WHO PREGENTION IS 2 stage Stage 1: preparetoty -anti influenza vacc to risk groups till end of october for 70% of population Specialisrs in hispitals for epidemics Stage 2: epidemic -isolation if pts to oregenr transmission Registering of pt Maskes for ots and workers changed EVERT 2 HRS Severe forms and complications are hospitals Isolation- close schools, stop planes, stop hospital visits Disinfection
38
Epi of echo and cocksackie
``` Dissemination -globally, Etio -belong to the enterovirus familiy of picornoviridae -rna viruses -32 serotypes 1-9’11-27, Grouos A 27 seroyrypes B 6 serotypes ``` Very stable to chloroform and bile due to lack of lipid Stable in environment 170 days and 160 days in lakes 7 days at room temp Sensitive to chlorone disinfection ``` Incubation 1-2 weeks Source Of infection Diseased and healthy carriers for 1-6 months ``` Polytropic viruses that affect many organs Echo Meningitis, rash, conjunctivitis ``` Cocksie A Aseotic me i gitis Heroes angina B Aseotic men Myocarditis and pericarditits ``` Exho and cocksakie can cause scute apathetic paralysis MOT - fecal oral route. Cont friits and veg. Canak water. - airborne is secondary like polio Susceptibility -mainly kids but new age frouos affect all ages Lethaliry - most are favourable unless CNS or heart is involvedwoth high lethaliry Seasons- summer to autum Prevention - no specific vaccine due to many serotypes - wash hands and avoid sick Epidemiological measures -dispensary surveillance Contacts -40 day observation Environment -disinfection and disinsection
39
Epi of cholera
Acute himan disease bt rubria cholera Fecal oral mechanisms History - bulgaria firsr time in 1883 - eradicated since 20’s 3 serotypes Classic has low stablity. Lasts a year Later type has hih srability but is sensitive to disinfection and high temp. Loc in lakes. Lasts 6 mo Source Diseased- end of incubarion oeriod and during sx. 30 litres released in feces Carriers Convalescence Iceberg phenomena Convalescence careiage is 7 days Healthy carriers excrete bac for 2 weeks max MOT -fecal oral Susceptibility is common. -immunocomp, poor nutrition. Active age ppl but longer period in kids No lifelong immunity Seasonlitt is summer b Prophylaxis - prevent movement from endemic regions - endemics more common caused by latter tyoes - many atypical forms so no vaccine Measures against disease -hospitalisarion in infectios ward. 3-ve samples taken 24 hrs after end of abiotic rx Contacts -isolated for 5 days w/ abiotic Environment -disnindectioin w/ chlorine