Diseases PIDSR

7/26/2019 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.


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.


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.


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


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

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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.


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


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.


+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.


#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


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.


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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.


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


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.


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.


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.


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.


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.


0 person ith acute diarrhea ith visible blood in the stool.


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.


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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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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To estimate the magnitude of the problem.

To determine trends and ris* factors associated ith the poisoning for the implementation ofprevention and control measures.


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.


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.


%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>


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+


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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Diseases PIDSR