Diseases PIDSR
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Transcript of Diseases PIDSR
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I. BACTERIAL AND
OTHER VIRAL DISEASES
Meningococcal Disease
Non-Neonatal TetanusInfluenza-lie Illness
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MENINGOCOCCAL DISEASE
Desc!i"tion#
Etiologic agent: Its an acute bacterial disease caused byNeisseria meningitidis
Mode of transmission: By direct contact (person to person), including respiratory droplets from
nose and throat of infected people. Incubation period:The average incubation period is 4 days, ranging beteen ! and "# days.
Period of communicabilit$ until live meningococci are no longer present in discharges from
nose and mouth.
!is" factors for se#ere disease and deat$: %ersons deficient in certain complement components
are especially prone to recurrent disease& splenectomi'ed persons are susceptible to bacteremic
illness. roupspecific immunity of un*non duration follos even subclinical infections.
I$"o!tance of Su!%eillance#
+eningococcal meningitis is the only form of meningitis to cause epidemics. The casefatality
rate is beteen - and "-. The maority of cases occur in children / years.
+eningococcal bivalent 0, 1 and 2uadrivalent 0, 1, 3, "5 vaccines are available&
immuni'ation of the entire population should be considered to halt epidemics due to 0 and 1
serogroup meningococci. Immuni'ation is also indicated for people traveling to endemic areas.6urveillance is needed to measure and detect epidemics and establish the impact of both
epidemic and nonepidemic disease
Stan&a!& Case Definition'Classification#
Sus"ecte& case# 0 person ith sudden onset of fever (758.91 rectal or 758.#91 aillary) and
one or more of the folloing:
- nec* stiffness
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- altered consciousness
- other meningeal signs
- petechial or purpural rash
- ;ote: In patients /" year, suspect meningitis hen fever is accompanied by bulging fontanels (!o)a)le case# 0 suspected case as defined above and: Turbid 16< (ith or ithout positive
ram stain) or ongoing epidemic and epidemiological lin* to a confirmed case. Confi!$e& case#0 suspected or probable case ith laboratory confirmation.
La)o!ato!* Confi!$ation#
%ositive 16< antigen detection or culture.
%ositive blood culture.
NON %NEONA&AL &E&AN'S
Desc!i"tion# Etiologic agent: Clostridium tetani, the tetanus bacillus
Mode of transmission: Tetanus spores are usually introduced into the body through a puncture
ound contaminated ith soil, street dust or animal or human feces& through lacerations, burnsand trivial or unnoticed ounds& or by inected contaminated drugs (e.g. street drugs). Tetanus
occasionally follos surgical procedures, hich include circumcision and abortions performed
under unhygienic conditions. The presence of necrotic tissue and=or foreign bodies favors grothof the anaerobic pathogen. 1ases have folloed inuries considered too trivial for medical
consultation. Incubation period:The incubation period usually 5$!" days, ith most cases occurring ithin
"4 days. 6horter incubation periods are associated ith more heavily contaminated ounds,more severe disease and a orse prognosis.
Period of communicabilit: ;o direct persontoperson transmission.
Susceptibilit and resistance: 6usceptibility is general. 0ctive immunity is induced by tetanus
tooid and persists for at least "# years after full immuni'ation& transient passive immunity
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follos inection of tetanus immune globulin (TI) or tetanus antitoin (e2uine origin). Infants
of actively immuni'ed mothers ac2uire passive immunity that protects them from neonatal
tetanus. >ecovery from tetanus may not result in immunity& second attac*s can occur andprimary immuni'ation is indicated after recovery.
!is" factors for se#ere disease and deat$: In general, shorter incubation periods are associated
ith more heavily contaminated ounds, more severe disease and a orse prognosis.
I$"o!tance of Su!%eillance# In developing countries, nonneonatal tetanus continues to be an important cause of preventable
morbidity and mortality. ;onneonatal tetanus also ta*es a terrible toll, especially in younger segments of the population.
It is estimated that in "??# about @# per cent of all nonneonatal tetanus cases and deathsoccurred among persons less than " years of age.
Stan&a!& Case Definition'Classification#
Sus"ecte& case#;ot applicable
(!o)a)le case#;ot applicable
Confi!$e& case# 0cute onset of hypertonia and=or painful muscular contractions (usually
muscles of the nec* and a) and generali'ed muscle spasms ithout apparent medical cause as
reported by a health care professional.
La)o!ato!* Confi!$ation#
Aaboratory confirmation is of little help because the organism is rarely recovered from the site of
infection and usually there is no detectable antibody response.
IN(L'EN)A%LI*E ILLNESS
Desc!i"tion#
0n acute viral disease of the respiratory tract characteri'ed by fever, headache, myalgia,
prostration, cory'a, sore throat and severe cough. Incubation period: usually "5 days and patient recovery is usually !$@ days.
Influen'a may be clinically indistinguishable from disease caused by other respiratory viruses,such as common cold, croup, bronchiolitis, viral pneumonia and undifferentiated acute
respiratory disease. Mode of transmission: through airborne spread among croded populations in enclosed spaces
herein the influen'a virus may persist for hours, particularly in the cold and in lo humidity. Transmission may also occur through direct contact. ;e subtypes may be transmitted globally
ithin 5$ months.
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!is" factors for se#ere disease and deat$: 6evere illness and death during annual influen'a
epidemics occur primarily among the elderly and those debilitated by chronic cardiac,pulmonary, renal or metabolic disease, anemia or immunosuppression.
I$"o!tance of Su!%eillance#
Cery important because of the rapidity ith hich influen'a epidemics develop, its etensivemorbidity and the seriousness of complications li*e viral and bacterial pneumonias.
Dssential for the early detection of ne viruses ith ne surface proteins that can cause
pandemics ran*ing as global health emergencies (e.g. "?"8, "?@, "?8) ith millions of deaths(c4# million in "?"8).
0llos for timely annual updates of a vaccine that can prevent deaths and alleviate illness in
vulnerable groups of the population
Stan&a!& Case Definition'Classification#
Sus"ecte& case# 0 person ith sudden onset of fever of E5891 and cough or sore throat in
the absence of other diagnoses. (!o)a)le case#;ot applicable
Confi!$e& case: 0 suspected case that is laboratoryconfirmed (used mainly in
epidemiological investigation rather than surveillance). Sus"ecte& Hu$an A%ian Influenza#0 suspect IAI case ith eposure to sudden bird
deaths (sudden bird deaths in two or more households in a barangay or death of at least
3% of commercial flock increasing twice daily for 2-3 consecutive days)F> confirmed
human avian influen'a case Sus"ecte& Se%e!e Acute Res"i!ato!* S*n&!o$e +SARS, case# 0 suspect IAI case ith
eposure to confirmed 60>6 case
La)o!ato!* Confi!$ation# Cirus isolation or %olymerase 1hain >eaction (%1>) of nasal=oropharyngeal sab or tracheal
aspirate from the suspected individual or direct detection of influen'a viral antigen or 4fold rise
in antibody titer beteen early and late serum
II+ MOS,'I&O%-O!NEPage 5of 25
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AND
)OONO&IC DISEASES
Acute .emorr$agic (e#er
Sndrome
Malaria
Leptospirosis
!abies
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AC'&E .EMO!!.AGIC (E/E! S0ND!OME
Desc!i"tion#
0 febrile syndrome associated ith bleeding manifestations.
0cute hemorrhagic fever syndromes can be attributable to dengue (dengue hemorrhagic fever),
Dbola+arburg viral diseases, Aassa fever, yello fever, >ift Calley fever, Gantavirus infections,1rimean1ongo hemorrhagic fever, and other viral, bacterial or ric*ettsial diseases ith a
potential to produce epidemics.
I$"o!tance of Su!%eillance#
The syndromic approach of the revised International Gealth >egulations (IG>), all cases of acute
hemorrhagic fever syndrome hether single or in clusters, should be notified early, ithout
aiting for the causal agent to be identified. 6urveillance of acute hemorrhagic fever syndrome is aimed at early detection of cases in order to
avoid epidemics and the possible international spread of the disease
Stan&a!& Case Definition#
0ny hospitali'ed person ith acute onset of fever of less than 5 ee*s duration and ith any
to of the folloing:
- hemorrhagic or purpuric rash
- epistais (nose bleeding)- hematemesis (vomiting of blood)
- hemoptysis (coughing out blood)- blood in stools
- other hemorrhagic symptoms
AND t$e diagnosis is not Dengue
La)o!ato!* Confi!$ation#
Isolation of organism through blood culture
Hetection of genomic se2uences by polymerase chain reaction (%1>)
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MALA!IA
Desc!i"tion# Etiologic agent: Guman malaria is caused by 4 species of proto'oan parasites of the genus
Plasmodium (P falci!arum,P viva",P malariae,P ovale).P falci!arum, the most prevalentspecies, is responsible for the maority of malaria deaths.
Mode of transmission:
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Susceptibilit: Susceptibility is universal ecept in humans ith specific genetic traits.
Tolerance or refractoriness to clinical disease is present in adults in highly endemic communitieshere eposure to infective anophelines is continuous over many years. +ost indigenous
populations of 0frica sho a natural resistance to infection ithP viva", hich is associated
ith the absence of Huffy factor on their erythrocytes. %ersons ith sic*le cell trait
(hetero'ygotes) sho relatively lo parasitemia hen infected ithP falci!arum, and thus arerelatively protected from severe disease& homo'ygotes suffering from sic*le cell disease are at
increased ris* of severe falciparum malaria, especially anemia. %ersons infected ith GIC are at
increased ris* of symptomatic falciparum malaria and its severe manifestations.
I$"o!tance of Su!%eillance#
+alaria is the most highly prevalent tropical disease, ith high morbidity and mortality and high
economic and social impact. The 4 elements of the lobal 6trategy for +alaria 1ontrol are:
- %rovision of early diagnosis and treatment,
- %lanning and implementing selective and sustainable preventive measures, including vectorcontrol,
-Darly detection, containment and prevention of epidemics,
- 6trengthening local capacities in basic and applied research to permit and promote the regular
assessment of a countrys malaria situation, in particular the ecological, social and economic
determinants of the disease.
Stan&a!& Case Definition'Classification#
#ncom!licated malaria$6igns and symptoms vary& most patients eperience fever. 6plenomegaly and
anemia are common associated signs. 1ommon but nonspecific symptoms include otherise
uneplained headache, bac* pain, chills, seating, myalgia, nausea, vomiting.
evere malaria: 1oma, generali'ed convulsions, hyperparasitemia, normocytic anemia, disturbances influid, electrolyte, and acidbase balance, renal failure, hypoglycemia, hyperpyreia, hemoglobinuria,
circulatory collapse=shoc*, spontaneous bleeding (disseminated intravascular coagulation) and
pulmonary edema.
In a!eas ITHOT access to la)o!ato!*-)ase& &iagnosis:
(!o)a)le unco$"licate& $ala!ia case#0 person ith signs (fever, splenomegaly, anemia)
and=or symptoms (uneplained headache, bac* pain, chills, seating, myalgia, nausea, vomiting)of malaria ho receives antimalarial treatment.
(!o)a)le se%e!e $ala!ia case: 0 person ho re2uires hospitali'ation for symptoms and signs of
severe malaria (coma, generali'ed convulsions, renal failure, hyperpyreia, circulatorycollapse=shoc*, spontaneous bleeding, and pulmonary edema) and receives antimalarial
treatment. (!o)a)le $ala!ia &eat/#death of a patient diagnosed ith probable severe malaria
In a!eas ITH access to la)o!ato!*-)ase& &iagnosis#
As*$"to$atic $ala!ia#0 person ith no recent history of symptoms and=or signs of malaria
ho shos laboratory confirmation of parasitemia.
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Confi!$e& unco$"licate& $ala!ia case#0 person ith signs (fever, splenomegaly, anemia)
and=or symptoms (uneplained headache, bac* pain, chills, seating, myalgia, nausea, vomiting)of malaria ho receives antimalarial treatment 0;H ith laboratory confirmation of diagnosis.
Confi!$e& se%e!e $ala!ia case#0 person ho re2uires hospitali'ation for symptoms and signs
of severe malaria (coma, generali'ed convulsions, hyperparasitemia, normocytic anemia,
disturbances in fluid, electrolyte, and acidbase balance, renal failure, hypoglycemia,hyperpyreia, hemoglobinuria, circulatory collapse=shoc*, spontaneous bleeding, disseminated
intravascular coagulation, and pulmonary edema) and receives antimalarial treatment 0;H ith
laboratory confirmation of diagnosis (microscopy or >HT). Confi!$e& $ala!ia &eat/#death of a patient classified as confirmed severe malaria.
Mala!ia T!eat$ent 0ailu!e# 0 patient ith uncomplicated malaria ithout any clear symptoms
suggesting another concomitant disease ho has ta*en a correct dosage of antimalarialtreatment, and ho presents ith clinical deterioration or recurrence of symptoms ithin "4 days
of the start of treatment, in combination ith parasitemia (aseual forms
La)o!ato!* Confi!$ation#
Hemonstration of malaria parasites in blood films (mainly aseual forms)
LEP&OSPI!OSIS
Desc!i"tion#
Etiologic agent: %athogenic leptospires belong to the genus&e!tos!ira (long cor*screshaped
bacteria, too thin to be visible under the ordinary microscope)& dar*field microscopy is re2uired.The more than !## pathogenic serovars clustered into ! serogroups cannot be differentiated on
the basis of morphology.
Mode of transmission: ild and domestic animals constitute the reservoir of infection,
transmitted through contact of mucous membranes or bro*en s*in ith ater, moist soil or
vegetation contaminated ith the urine of infected animals (simming or immersion)&
occasional infection occurs through ingestion=inhalation of food=droplet aerosols of fluidscontaminated by urine.
Incubation period:The incubation period is usually "# days ith a range of !$5# days.
Period of communicabilitKduring acute infection and until the infectious agent is no longer
present in feces, usually ithin 4 ee*s after illness. 0symptomatic carriers may transmit
infection& rarely, the carrier state may persist for months or longer. 0ppropriate antimicrobial
treatment usually reduces duration of carriage to a fe days. Hirect persontoperson
transmission is rare. Aeptospires may be ecreted in the urine, usually for " month, althoughleptospiruria has been observed in humans and in animals for months, even years, after acute
illness. Susceptibilit:6usceptibility of humans is general& serovarspecific immunity follos infection
or (occasionally) immuni'ation, but this may not protect against infection ith a different
serovar.
I$"o!tance of Su!%eillance#
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6urveillance provides the basis for intervention strategies in human or veterinary public health.
Aeptospirosis is probably underreported in many countries because of difficult clinical diagnosis
and lac* of diagnostic laboratory services.
Stan&a!& Case Definition'Classification#
Sus"ecte& case#0 person ho developed acute febrile illness ith headache, myalgia andprostration associated ith any of the folloing:
- conunctival suffusion, meningeal irritation, anuria or oliguria and=or proteinuria,
- aundice, hemorrhages (from the intestines or lungs), cardiac arrhythmia or failure,
- s*in rash
A(&E!eposure to infected animals or an environment contaminated ith animal urine (e.g. ading
in flood aters, rice fields, drainage).
(!o)a)le case#;ot applicable
Confi!$e& case#0 suspect case that is laboratory confirmed
La)o!ato!* Confi!$ation#
Isolation (and typing) from blood or other clinical materials through culture of pathogenic
Aeptospira. %ositive serology, preferably +icroscopic 0gglutination Test (+0T), using a range of Aeptospira
strains for antigens that should be representative of local strains
!A-IES
Desc!i"tion#
Etiologic agent: The rabies virus, a rhabdovirus of the genus&yssavirus.
Mode of transmission: Gosts are usually Canidae, including dogs (responsible for more than
??- of all human deaths from rabies), foes, coyotes, olves, and ac*als& also cats, s*un*s,raccoons, mongooses, bats, and other biting animals. 0 bite or a scratch introduces virusladen
saliva from a rabid animal. Incubation period:The incubation period is usually 58 ee*s but maybe as short as ? days and
as long as @ years Period of communicabilit: In dogs and cats, usually for 5$@ days before onset of clinical signs
(rarely over 4 days) and throughout the course of the disease. Aonger periods of ecretion beforeonset of clinical signs ("4 days) have been observed ith Dthiopian dog rabies strains. In one
study, bats shed virus for "! days before evidence of illness& in another, s*un*s shed virus for at
least 8 days before onset of clinical signs. 6*un*s may shed virus for up to "8 days before death.
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Susceptibilit: In dogs and cats, usually for 5$@ days before onset of clinical signs (rarely over 4
days) and throughout the course of the disease. Aonger periods of ecretion before onset ofclinical signs ("4 days) have been observed ith Dthiopian dog rabies strains. In one study, bats
shed virus for "! days before evidence of illness& in another, s*un*s shed virus for at least 8 days
before onset of clinical signs. 6*un*s may shed virus for up to "8 days before death.
I$"o!tance of Su!%eillance#
6urveillance of both human and animal rabies is essential to 2uic*ly detect outbrea*s in endemic
areas and ne cases in rabiesfree area. Hetermine high ris* areas for intervention purposes
+onitor the use of vaccine and immunoglobulin.
Dvaluate effectiveness of intervention at the level of the animal reservoir and eposed human
population.
Stan&a!& Case Definition'Classification#
Sus"ecte& Case#0 person presenting ith an acute neurological syndrome (encephalitis)
dominated by forms of hyperactivity (furious rabies) or paralytic syndromes (dumb rabies) thatprogresses toards coma and death, usually by respiratory failure, ithin @ to "# days after the
first symptom if no intensive care is instituted. (!o)a)le case#0 suspected case plus history of contact ith suspected rabid animal.
;ote: Bites or scratches from a suspected animal can usually be traced bac* in the patient
medical history. The incubation period may vary from days to years but usually falls beteen 5#
and ?# days.
Confi!$e& case#0 suspected case that is laboratory confirmed.
La)o!ato!* Confi!$ation#
Hetection of rabies viral antigens by direct fluorescent antibody (
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III+ (ood%borne Diseases
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0cute Bloody Hiarrhea
1holera
%aralytic 6hellfish %oisoning Typhoid and %aratyphoid
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S/igellosis
Etiologic agent: Its a bacterial disease caused by higella dysenteriae '(6higa bacillus)
Mode of transmission: By direct contact (person to person) or contaminated food or ater. Incubation period:Jsually "$5 days, but may range from "! to ? hours& up to " ee* for
dysenteriae ". Period of communicabilitKduring acute infection and until the infectious agent is no longer
present in feces, usually ithin 4 ee*s after illness. 0symptomatic carriers may transmit
infection& rarely, the carrier state may persist for months or longer. 0ppropriate antimicrobialtreatment usually reduces duration of carriage to a fe days.
!is" factors for se#ere disease and deat$: The disease is also most li*ely to be severe, and the
ris* of death greatest, among: infants, and adults older than # years&
children ho are not breastfed&
children recovering from measles& malnourished children and adults& and
any patient ho develops dehydration, unconsciousness or hypo or hyperthermia, or has
a history of convulsion hen first seen.
I$"o!tance of Su!%eillance#
The emergence of strains of higella dysenteriae type " resistant to most antibiotics has become
a maor public health concern. The high casefatality and the epidemic potential ma*e surveillance to detect and control the
outbrea*s essential.
Stan&a!& Case Definition'Classification#
0 person ith acute diarrhea ith visible blood in the stool.
La)o!ato!* Confi!$ation#
Aaboratory culture of stools may be used to confirm possible outbrea*s of specific diarrhea, such
as 6higella dysenteriae type ", but is not necessary for case definition. %atients for culture should be chosen among those ith bloody diarrhea for less than 4 days,
ithout treatment, ho agree to the eamination.
Bacterial: ram stain, fecal leu*ocytes, culture, antimicrobial susceptibility, 6erotyping, toinidentification
%arasitic: macroscopic and microscopic eamination
Ciral: 0ntigen Hetection
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C.OLE!A
Etiologic agent: ibrio cholerae serogroups F" and F"5?. 6erogroup F" occurs as to
biotypes$ classical and Dl Tor$each of hich occurs as 5 serotypes (Inaba, Fgaa and rarelyGi*oima). The clinical pictures of illness caused by cholerae F" of either biotype and
cholerae F"5? are similar because an almost identical enterotoin is elaborated by these
organisms.
Mode of transmission: 1holera is ac2uired through ingestion of an infective dose of
contaminated food or ater and can be transmitted through many mechanisms.
Incubation period:egulations.
Stan&a!& Case Definition'Classification#
Sus"ecte& case:
- Disease unno1n in t/e a!ea#0 person aged years or more ithsevere dehydration or ho
died from acute atery diarrhea, O!- Disease en&e$ic in t/e a!ea#0 person aged years or more ith acute atery diarrhea ith or
ithout vomiting, O!
- In an a!ea 1/e!e t/e!e is a c/ole!a e"i&e$ic# 0 person ith acute atery diarrhea, ith or
ithout vomiting.
(!o)a)le$;ot applicable Confi!$e& case$ 0 suspected case that is laboratoryconfirmed.
Note$ Cholera does a!!ear in children under years* however+ the inclusion of all cases of acute
watery diarrhea in the 2-, year age grou! in the re!orting of cholera greatly reduces the s!ecificity
of re!orting or management of cases of acute watery diarrhea in an area where there is a cholera
e!idemic+ cholera should be sus!ected in all !atients
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La)o!ato!* Confi!$ation#
Isolation of ibrio cholerae #" or #"5? from stools in any patient ith diarrhea.
PA!AL0&IC S.ELL(IS. POISONING
Is t$ere an antidote for PSP1
No+ %6% is a neurotoin that bloc*s movement of sodium through membranes of nerve cells. ithout
sodium transmission, nerve cells cannot function. This leads ultimately to the symptoms of %6%:
numbness, paralysis, respiratory failure, and coma. There is no specific antidote to stop the effect of%6% toicity.
Is t$ere a treatment for PSP1
0es+ Induce vomiting by stic*ing a finger don the throat, drin*ing arm saltater or ta*ing 6yrup
of Ipecac to epel shellfish from the victims stomach. Treat the victim for shoc* and transport to a
medical facility. 0pplication of life support services at the medical care facility may be necessary tosustain the life of the victim. >eduction of symptoms normally occurs ithin ? hours and complete
recovery usually ithin !4 hours. 3ou must not underestimate the seriousness of %6%. Fnce the
symptoms begin to appear, the victim must be transported immediately to a medical care facility.
Does coo"ing eliminate PSP from s$ellfis$1
No+ %6% toins are heat stable. Dven hen pressure coo*ed at a temperature of !# o< for "
minutes, %6% remains toic.
Can I test for PSP in s$ellfis$ b c$e2ing a small piece of s$ellfis$ tissue and see if I feel tingling in
m lips1 If no tingling or numbness occurs3 is t$e s$ellfis$ O* to eat1
1heing on a small piece of shellfish gives you no clue as to the %6% dosage in the tissue. In
addition, %6% toins in an acid pG environment undergo chemical transformations that may producemore potent toins than originally found in the shellfish. 6ince your mouth has a nearly neutral pG,
the toins in your mouth may not have the potency as the toins that are formed in acidic conditions
of your stomach.
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I$"o!tance of Su!%eillance#
To estimate the magnitude of the problem.
To determine trends and ris* factors associated ith the poisoning for the implementation ofprevention and control measures.
Stan&a!& Case Definition'Classification#
Sus"ecte& case#0 person ho develops one or more of the folloing signs and symptoms after
ta*ing shellfish meal or soup:
- ensory $paresthesias (tingling sensations on s*in), numbness (lac* of sensation) of the oralmucosa and lips, numbness of the etremities
- .otor$difficulty in spea*ing, salloing, or breathing, ea*ness or paralysis of the etremities (!o)a)le Case#;ot applicable
Confi!$e& case#0 suspected case in hich laboratory tests (biologic or environmental) have
confirmed eposure.
La)o!ato!* Confi!$ation#
Hetection of saitoin in epidemiologically implicated food, serum or urine of cases.
&0P.OID AND PA!A&0P.OID (E/E!
Desc!i"tion
Etiologic agent: In the recently proposed nomenclature for almonella the agent formerly
*non as ty!hi is called enterica subsp. enterica serovar Typhi (commonly Typhi).
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f) 0bout idal Test: Ideally, the idal test should be run on both acute and convalescent
phase sera to detect an increase in the agglutination titer. The results from a single sample are
difficult to interpret because high bac*ground rates of circulating antibodies to serotypeTyphi or other almonella serotypes may produce a falsepositive result. In areas of high
endemicity, a single idal test can lead to many falsepositive and falsenegative results.
Fperator variability also contributes to unreliable results.g) 0bout Typhidot: This test ma*es use of the # *H antigen to detect specific Ig+ and Ig
antibodies to ty!hiThe detection of Ig+ reveals acute typhoid in the early phase of
infection, hile the detection of both Ig and Ig+ suggests acute typhoid in the middlephase of infection. In areas of high endemicity here the rate of typhoid transmission is high
the detection of specific Ig increases. 6ince Ig can persist for more than to years after
typhoid infection the detection of specific Ig cannot differentiate beteen acute and
convalescent cases.
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IC. FTGD> HI6D06D6
%ertussis
Hiphtheria
G
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PE!&'SSIS
D esc!i"tion#
Etiologic Agent:%ertussis or hooping cough is a highly communicable disease of the respiratory tract
causes by Bordetella %ertussis.
The initial stage of the disease has an insidious onset ith an irritating cough that gradually becomes
paroysmal, usually ithin "! ee*s, and lasts for "! months.
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%aroysms are characteri'ed by repeated violent cough. Dach series of paroysms has many cough
ithout intervening inhalations and can be folloed by a characteristic croning or highpitched
inspiratory hoop. %aroysms fre2uently end ith the epulsion of clear, tenacious mucus, oftenfolloed by vomitingP
Mode of transmission:By direct contact ith airborne discharged from the mucus membrane of infected
person or indirect contact through articles freshly soiled ith discharges of infected persons.
Incubation Period:The average is ?"# days ranging from to !# days.
I$"o!tance of Su!%eillance#
%ertussis is a maor cause of childhood morbidity and mortality. 1aseQfatality rates in developing
countries can reach "-.
6urveillance data on the disease can monitor the impact of vaccination on disease incidence. Identify high
ris* areas and identify outbrea*s
Stan&a!& Case &efinition#
Clinical Case
0 person ith a cough lasting at least ! ee*s ith at least one of the folloing:
%aroysms (i.e. fits) of coughing Inspiratory hooping
%osttussive vomiting (i.e. vomiting immediately after coughing)
ithout other apparent cause.
Case classification#
Clinicall%confirmed case:
0 case that meets the clinical case definition but is not laboratory confirmed.
Probable case:
+eets the clinical case definition, is not laboratory confirmed, and is not epidemiologicallylin*ed to a laboratoryconfirmed case.
Laborator%confirmed case:
0 case of acute cough illness of any duration ith a positive culture for B. pertussis& F>
0 case that meets the clinical definition and is confirmed by %1>& F>
0 case that meets the clinical definition and is epidemiologically lin*ed directly to a case
confirmed by either culture or %1>
La)o!ato!* Confi!$ation#
Isolation of Bordetella pertussis, or detection of genomic se2uences by polymerase chain
reaction (%1>). 6pecimen: nasopharyngeal sab using >eaganAoe it.
DIP.&.E!IA
D esc!i"tion#
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Hiphtheria is an infectious disease that usually affects the tonsils, pharyn, laryn and occasionally other
mucus membranes or s*in.
Mode of transmission:spread (from person to person) by direct contact to respiratory droplets through
coughing and snee'ing if infected persons.
Incubation Period:usually ! to days (range ""# days)
I$"o!tance of Su!%eillance# Hiphtheria is a idespread severe infectious disease that has potential for epidemics. The control of
diphtheria is based on the folloing measures:
Primar pre#entionof the disease by ensuring high population immunity through immuni'ation Secondar pre#entionof the spread through rapid investigation of closed contacts. In order to ensure
proper treatment.
&ertiar pre#entionof complications and deaths through early diagnosis and proper management.
The purposes of diphtheria surveillance reports are:
To assist in the diagnosis of cases and ensure prompt and appropriate treatment. To prevent outbrea*s or limit their scope by timely identification of contacts, and provision
of appropriate prophylais&
To help guide an appropriate communityide response if a diphtheria outbrea* occurs.
0ny probable or confirmed case must be investigated.
6urveillance data can be used to monitor levels of immuni'ation coverage (target 7?-) and
disease as a measure of the impact of control program. >ecent epidemics have highlighted the
need for ade2uate surveillance and epidemic preparedness.Stan&a!& Case &efinition#
Probable case:
0 person ith an illness of the upper respiratory tract characteri'ed by laryngitis or pharyngitis
or tonsillitis, and adherent membranes on tonsil, pharyn and= or noseConfirmed case:
0 case that is laboratory confirmed or lin*ed epidemiologically to a laboratoryconfirmed case.
Note: persons 2it$ positi#e Cornebacterium dipt$eriae cultures 2$o do not meet t$e
clinical description 5i+e+ asmptomatic carriers6 s$ould not be reported as probable or
confirmed dip$t$eria cases+
La)o!ato!* Confi!$ation#
Isolation of 1orynebacterium diphtheria from a clinical specimen. Because diphtheria can
progress rapidly, the initial diagnosis must be made on the basis of clinical presentation so that
the presumptive therapy can be started 2uic*ly.
6pecimens for culture should be obtained as soon as diphtheria is suspected, even if treatment
ith antibiotics has already begun. 6abs should be ta*en from the nose and throat, ith care to
sab under the edge of the membrane, if present.
Note: a rise in serum antibod 5fourfold or greater6 is of interest onl if bot$ serum samples2ere obtained before administration of dip$t$eria to7oid or antito7in+ &$is is not usuall
t$e case in sur#eillance3 2$ere serological diagnosis of dip$t$eria is t$us unli"el to be an
issue.
.AND3 (OO&3 8 MO'&. DISEASE
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