13053_Typhoid Food Poisioning Malaria

8/8/2019 13053_Typhoid Food Poisioning Malaria

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Typhoid fever

Caused by Salmonella enterica subtype

Typhi

Acquired by ingestion of food or watercontaminated by feces of infected humans

or person to person contact.

In earlier centuries the disease occurred in

great epidemics.


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A milder form of disease , paratyphoidfever, is caused by Paratyphi A,B and C ofSalmonella enterica subspecies enterica.

In small intestine, the incubation period isabout 10 to 14 days.

The bacteria colonize the small intestine,

penetrate the epithelium and spread to thelymphoid tissue, blood , liver and gallbladder.


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Symptoms include fever, headache,

abdominal pain, malaise, which last for

several weeks. Bacteria then reinfect the gastrointestinal

tract, producing abdominal pain and

diarrhea.


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After approximately 3 months, most

individuals stop shedding bacteria in their

feces. However, a few individuals continue to

shed S.Typhi for extended periods but

show no symptoms.


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Lab diagnosis of typhoid fever is by

demonstration of typhoid bacilli in the

blood, urine or stools and serology. Treatment with ceftriaxone or ciprofloxacin

has reduced the mortality rate to less than

1%.

Recovery from typhoid confers a

permanent immunity.


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Purification of drinking water, prevention of

food handling by carriers , complete

isolation of the patients are the mostsuccessful preventive measures


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Food Poisoning

Types

Nan bacterial

By chemical agents, or chemical poisons like

pesticides, fertilizers, poisonous plants,chemicals etc.

Bacterial

Salmonella

E. coli

Staphylococcal food poisoning

Botulism


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Food Poisoning

Staphylococcal food poisoning is the major type

of food intoxication.

It is caused by ingestion of improperly stored or

cooked food in which Staphylococcus aureus

has grown.

S.aureus a gram positive coccus is very

resistant to heat, drying and radiation It is found in the nasal passage and on the skin

of humans and other mammals worldwide.


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If the bacteria are allowed to incubate in

certain foods, they produce heat stable

enterotoxins that render the food

dangerous even though it appears normal

Once the bacteria has produced the

toxin,the food can be extensively and

properly cooked,killing the bacteria withoutdestroying the toxin.


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Intoxication can result from the food that

has been throughly cooked.

13 different enterotoxins have beenidentified; enterotoxins A,B,C1,C2,D and E

are the most common

These toxins appear to act as neurotoxins

that stimulate vomiting though the vagus

nerve.


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Typical symtoms include severeabdominal pain, cramps,diarrhea, vomitingand nausea

The onset of the symptoms is rapid (usually 1 to 8 hrs) and of short duration(usually less than 24 hrs)

Mortality rate of staphylococcal foodpoisoning is negligible among healthyindividuals.


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E.Coli infections

Large percentage of travelers acquire a

rapidly acting, dehydrating conditions

called travelers diarrhea.

This condition results from an encounter

with certain viruses, bacteria or protozoa

usually absent from travelers normal

environment.

One of the major causative agent is E.coli


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This bacterium circulates in the resident

population , typically without causing

symptoms due to the immunity afforded by

previous exposure

Contaminated food and water are the

major means by which the bacteria can

spread


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Botulism

Agent: Enterotoxin of Closteridium

bodulinum of type A, B, E

Source: soil, dust and intestinal tract of

animals.


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Prevention and cure

Food sanitation

Personal hygiene

Meat inspection Protective storage

Refrigeration

Laboratory analysis of food material fromrestaurants form time to time


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Treatment

With held solid food

Combat dehydration by intravenous fluid

supply Antibiotics like ampicillin, co-trimoxazole,

erythromycin

Codiene phosphate and loperamide areuseful in controlling diarrhoea.


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Malaria

Most important human parasite among theprotozoa is Plasmodium, the causativeagent of malaria.

Human malaria is caused by four speciesof Plasmodium : P.falciparum,P.malariae,P.vivax and P. ovale

The parasite first enters the bloodstreamthrough the bite of an infected femaleAnopheles mosquito


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Malaria life cycle


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As she feeds, the mosquito injects a small

amount of saliva containing an

anticoagulant along with small

sporozoites.

The sporozoites in the bloodstream

immediately enter hepatic cells of liver

In the liver they undergo multiple asexual

fission and produces merozoites.


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After being released from the liver cells,the merzoites attach to erythrocytes andpenetrate these cells.

Once inside the erythrocyte, thePlasmodium begins to enlarge as atrophozoite.

The trophozoite nucleus then dividesasexually to produce a schizont that has 6to 24 nuclei.


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The schizont divides and producesmononucleated merozoites.

Eventually the erythrocyte lyses, releasingthe merozoites into the bloodstream toinfect other erythrocytes

This erythrocytic stage is cyclic and

repeats itself app every 48 to 72 hrs orlonger, depending on the species ofPlasmodium involved.


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Sudden release of merozoites,toxins and

erythrocyte debris triggers an attack of the

chills,fever and sweats characteristic of

malaria.

Occasionally merozoites differentiate in

macrogametocytes and

microgametocytes, which do not rupturethe erythrocytes.


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When these are ingested by a mosquito,

they develop into female and male

gametes,respectively.

In the mosquito gut the infected

erythrocytes lyse and gametes fuse to

form a diploid zygote called the ookinete

The ookinete migrate to the mosquito gut

wall,penetrates and form a oocyst.


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In the process called sporogony, the oocystundergoes meiosis and forms sporozoites,which migrate to the salivary glands of the

mosquito. The cycle is complete and when the mosquitoe

bites another human host and cycle beginsanew.

The pathological changes caused by malariainvolve not only the erythrocytes but also thespleen and other visceral organs


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Classic symptoms first develop with thesynchronized release merozoites anderythrocyte debris into the bloodstream,resultingin shaking chills,then burning fever followed by

sweating. It may be that the fever and chills are caused

partly by a malarial toxin that inducesmacrophages to release TNF- alpha andinterleukin 1

After one attack there is a remission that lastsfrom a few weeks to several months, then thereis a relapse


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Anemia can result from the loss of

erythrocytes

Children and nonimmune individuals candie of cerebral malaria.


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Mode of transmission

Vector transmission

Direct transmission through blood

Congenital i.e. from mother to new born

Incubation period: 9- 30 days


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Clinical features

Cold stage: sudden onset of fever, chills

and sensation of extreme cold. Lasts for

15min to hr

Hot stage: temp rise upto 106rF. lasts for

2-6 hrs

Sweating stage: lasts for 2-4 hrs


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Diagnosis

Made by demonstrating the presence of

parasites within giemsa stained

erythrocytes.

When blood serums are negative,

serological testing can establish a

diagnosis of malaria

Treatment includes administration of

chloroquine


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Prevention and control

Protection against mosquito bite likemosquito repellent, protective clothing,bed net etc.

Anti larval measure like (larvicides) likekerosine oil & gambusia fish

Anti adult mosquito measure (inseticide)

like DDT,F

lit etc Control of human reservoir

(chemoprophylaxis) drugs like choloroquin

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13053_Typhoid Food Poisioning Malaria