SlideShare a Scribd company logo
Epidemiology of common
infectious diseases
This Photo by Unknown Author is licensed under CC BY-SA-NC
RESPIRATORY INFECTIONS
• SMALL POX
• HUMAN MONKEYPOX
• CHIKENPOX
• MEASLES
• RUBELLA
• MUMPS
• INFLUENZA
• DIPHTERIA
• PERTUSIS
• ARI
• COVID 19
• TUBERCULOSIS
SMALL POX
Caused by variola virus
Acute onset of fever,headache,back ache, vomiting
Rash on day 3 – centrifugal distribution
Macule – papule – vesicle – pustule – scab – scarring
Eradicated on 1977 ; last case in India 1977
HUMAN MONKEY POX
viral zoonosis
Genus orthopoxvirus
Natural hosts – squirrels , rodents , non human primates
etc
Transmission :
Animal to human
Direct contact with blood ,body fluids of infected
animals.
Eating animal products of infected animals
Human to human: droplet infection , skin lesions
Incubation period : 5 to 21 days
Clinical picture :
Fever, head ache, lymphadenopathy ,myalgia
Rash on 3rd day – more on face and extremities
Self limited disease
Diagnosis : PCR (vesicle fluids/dry crusts)
Management : symptomatic treatment , managing
complications, preventing long term sequels.
Prevention : awareness of risk factors
health education
Complications : secondary infections , bronchopneumonia
,sepsis, encephalitis , corneal infection.
CHICKENPOX
• Agent : varicella zoster virus/human alpha herpes virus 3
• Primary infection cause chickenpox
• Recovery followed by latent infection.
• Reactivation results in zoster- a painful, vesicular, pustular
eruption in distribution of one or more sensory nerve roots.
Incubation Period: Usually 14-16 days, although extremes as
wide as 7-21 days have been reported.
Transmission :Droplet infection and droplet nuclei.
“Face to face” (personal) contact.
Portal Of Entry: Respiratory tract.
rash
Eruptive Stage:
Symmetrical.
Appears on the trunk and
then comes to face, arms
,legs.
Mucosal surfaces (buccal,
pharyngeal) are generally
involved.
Axilla may be affected. Palms
and soles usually not
involved.
The density of eruption
diminishes centrifugally.
Rapid evolution:
Stages of-macule - papule -
vesicle - scab.
Dew drops appearance of
vesicles.
Superficial in site, with easily
ruptured walls and surrounded
by inflammation.
• Vesicles form crusts
• Scabbing begins 4-7 days
after the rash appears.
CONTROL:
No specific treatment for chicken pox.
Notification.
Isolation of cases for about 6 days after onset of rash.
Disinfection of articles soiled by nose and throat discharges.
VARICELLA ZOSTER IMMUNOGLOBULIN(VZIG):
VZIG given within 72 hours of exposure has been
recommended for prevention.
DOSAGE:1.25-5ml intramuscularly.
MEASLES
• Measles is a highly contagious, acute, exanthemata's
respiratory disease, with characteristic clinical picture and
pathognomonic exanthem “koplik’s spots
• Clinically characterized by fever and catarrhal symptoms of
upper respiratory tract (coryza, cough), followed by typical
rash.
Epidemiological factors:
AGENT:
• RNA ParamyxoViruses.
• Only one serotype known.
• Cellular receptors for measles virus are CD46,CD156
expressed on Human lymphocytes.
Genus: MORBILLI
Family: Paramyxoviridae
• Measles virus in droplet nuclei invade respiratory epithelium and
attack reticuloendothelial system.
SOURCE OF INFECTION:
• Only case of measles
• No carriers
• No sub-clinical infections
Infective material
• Secretions from nose, throat and respiratory tract during prodromal
period and early stages of rash.
COMMUNICABILITY
Highly infectious during prodromal period and at the time of
eruption.
Period of communicability:
4 days before the onset of rash to 5 days
after the appearance of rash.
Secondary attack rate:
depends on susceptible children.

Host Factors

NUTRITION:Mortality due to measles in malnourished child is 400
times more than in well nourished cases.
 Malnourished children excrete the virus for prolonged periods. So
they are dangerous to the community.
ENVIRONMENTAL:WINTER disease.
India- winter and early spring. (i.e. Jan-April.)
SOCIOECONOMIC FACTORS:
poverty-malnutrition-low cell mediated immunity-prone to severe
measles-increased mortality
IMMUNITY: One attack gives lifelong immunity.
Second attacks rare.
Infants protected by maternal antibodies up to 6 months.
Vaccination gives lifelong immunity.
Transmission
Direct
Droplet infection.
Droplet nuclei.
Portal of entry: Respiratory tract
Infection through conjunctiva also seen
 Virus remains active and contagious in air or infected surface for
up to 2 hr.
 Recipients of vaccine are not contagious to others.
Incubation Period
10 days from exposure to onset of fever and 14 days to appearance of
rash.
RUBELLA
• Toga virus
• RNA virus
• Rapidly inactivated by chemicals light, low Ph,
heat.
• Reservoir: Human
• Transmission:Respiratory,Subclinicalcases
Communicability:7 days before and to 5-7 days after rash.
Infants with CRS may shed virus for a year or more.
• Incubation period 14 days(range 12-23 days)
• Prodrome of low - grade fever
• Lymphadenopathy in second week.
• Maculo-papular rash 14-17 days after exposure.
• Congenital rubella syndrome : hearing impairment
congenital heart defect
cataract
• Rubella vaccine: Live viral vaccine RA 27/3
• Indications: All infants 12 months of age and older.
• Susceptible adolescents and adults without documented
evidence of rubella immunity.
• Emphasis on nonpregnant women of childbearing age,
particularly those born outside the U.S.
MUMPS
Mumps is an acute infectious disease caused by a virus which has a
predilection for glandular and nervous tissue.
EPIDEMIOLOGY
Agent factors:
Myxovirus parotidis
Source:clinical and
subclinical cases
Period of
communicability:4-6
days before symptoms
and a week thereafter.
Secondary attack rate
:86%
Host factors:
5-15 years
More severe in
adults
One attack confers
lifelong immunity
i
Environmental
factors
Endemic
Peak in winter
and spring
overcrowding
Mode of transmission:droplet infection
IP:2 to 3 weeks(18days)
Clinical features :
pain and swelling of one or both parotid glands
fever
earache
pain or stiffness on opening mouth
swelling subsides over 1-2 weeks
complications : orchitis , oophoritis , encephalopathy
INFLUENZA
Acute respiratory infection caused by influenza A,B,C,D viruses
Sudden onset of malaise,chills,fever,muscle pain,cough
1918 Spanish influenza
1957 Asian influenza
1968 Hong Kong influenza
2009 Swine flu/H1N1
Presently circulating – A(H1N1),A(H3N2),B(H3N2)
•The virus is spreading rapidly reaching all continents less than 3
months due to the speed of international air travel today.
•Epidemiologic determinants
AGENT:
Family Orthomyxoviridae
There are 3 types :
Type A
Type B
Type C
Antigenically distinct
No cross immunity
Reservoir of infection:Mainly - Animals & Birds
Some include H and N antigens related to humans
New strains by recombination influenza virus between man animals
birds.
•Host Factors:Usually case are subclicinal case.
Nasal secretions are infective.
• During epidemics,large number of mild and Asympomatic occurs
play an important role in spread of infection.
(A) Age and Sex:
All ages and both sexes
Highest mortality rate amount certain high
risks groups.
Example: Old people children under 18 months ,diabetes, or CHD.
(B) Human Mobility :
Important factors in spread of infection.
(C) Immunity :
Subtype specific
Antibodies against HAAND NA
Antibodies appear about 7 days after the attack and reach maximum
level in about 2 weeks after 8 to 12 months,level drops to pre infection
level.
(D)Environmental factors:
Season
overcrowding
Mode of transmission: Persons to persons by droplet
infection or nuclei created by sneezing, coughing, talking.
The portal of entry of virus is respiratory tract.
Incubation period: 18 to 72 hours
Complications :
Pneumonia ,Guillain Barre syndrome ,Reye Syndrome ,Fatty
liver.
Lab diagnosis: virus isolation from nasopharyngeal
secretions
Govt. of India. influenza virus centre, Pasteur institute Coonoor,
South India, Haffkine institute, Mumbai,School of tropical Medicine
(Kolkotha),AIIMS (New Delhi,Vallabhai Patel Chest institute (Delhi),
Armed Forces Medical College (Poone)
Prevention :
Take precautions
• Good ventilation of public buildings.
• Avoidance of crowded places during epidemics.
• Encouraging suffers to cover their faces.
• 7 stays at home at the sign of influenza.
• Hygienic practices during handling of poultry products including:
• hand washing, prevention of cross contamination and thorough
cooking to > 70 ' c of poultry products.
• Influenza vaccines
Diphtheria
Acute infectious and communicable disease characterized by
involvement of the respiratory system, the local production of
membrane and general symptoms caused by absorption of toxin .
Agent: Cornybacterium diphterium
Gram positive, Non sporing, Non capsulated and non motile, slender
rod shaped bacteria.
nasal
Case carrier
throat
Case : Range from sub clinical to frank clinical cases .
Temporary Carrier : State may last for about a month .
Permanent Carrier : State may persist for a year or so unless the
patient is treated.
Source of infection
Infective Material
Nasopharyngeal Secretions .
Discharge from Skin Lesions .
Contaminated fomites and possibly infected Dust.
Period of Infectivity
Cases - 14 to 28 days
Carriers - Longer periods
Mode of transmission
Mainly by droplet infection . ►
Infected cutaneous lesions .
By objects (ex : Cups, Thermometers) contaminated by the
nasopharyngeal secretions of the patient
Portal Of Entry
Respiratory Route – Most common.
Non respiratory routes
~ Skin – cuts, wounds & Ulcers.
~ Umbilicus of new born.
~ Eye, genitalia and middle ear.
Incubation Period
~ 2 – 6 Days.
Pertussis
Whooping cough (pertussis)is an acute infectious disease,
usually of young children caused by the bacteria bordetella pertussis.
The Chinese call it a “Hundred Day Cough”.
Agent
Bordetella pertussis,Small gram negative,Aerobic coccobacillus
Source
•B.pertussis infects only man
•S.O.I is a case of pertussis
Infective material
•Nasopharyngeal and bronchial secretions – bacilli occurs more in
number.
Infective period
•Catarrhal stage
Host Factors:
Age-Disease of infants and
preschool children
•Highest incidence – below 5 years
•High mortality - Infant below 6 months
Environmental factors:
Through out the year
More cases – winter and spring
Risk greater in lower social classes
Infection generally lasts 2 to 3 weeks with 3 stages
Catarrhal Stage
• mild cough
• Running nose
• low grade fever
• lasts for about 10
days
Paroxysmal stage
cough gets worse. cough is dry
and harsh.cough ends with
whoop sound on
inspiration.child may vomit
with the coughing and appear
to be strangling on the
vomit.cough can be started by
many factors, including
feeding, crying, or playing.
Convalescent stage
Vomiting and the
whooping cough
cease first. The
cough usually
decreases around the
sixth week, but may
continue on occasion
for the next one to 2
months.
Control
Cases and contacts
i. Cases
Early diagnosis,isolation
and treatment of cases and
disinfection of discharges.
Antibiotics – erythromycin,
ampicilin, septran or
tetracycline useful in
controlling secondary
bacterial infection
ii. Contacts
Infants and young children
kept away.
Those known to have been
in contact – prophylactic
antibiotic – days.
iii.DPT vaccine
Tuberculosis
The Mycobacterium tuberculosis belongs to the genus Mycobacterium.
• aerobic,
• non motile,
• rod-shaped bacteria.
• Two distinguishing characteristics :
• acid alcohol-fastness (AAFB), so strongly resistant,
• slow growth.
• Pulmonary TB is the most frequent presentation,
• -Extra-pulmonary TB (e.g. miliary, skeletal, meningeal,
gastro-intestinal) also occur,
• particularly in children
• immigrants and impaired immunity
Primary TB develops within 1 or 2 years after an initial infection and,
particularly in children, is often associated with disseminated disease.
Post-primary TB develops later in life, and can be caused either by
reactivation of bacteria remaining from the initial infection or by
failure to control a subsequent reinfection.
Post-primary TB is predominantly a pulmonary disease, involving
extensive damage to the lungs and efficient aerosol transmission of
bacteria.
The risk of disease is highly dependent on:
•the immune status of the host
•co infection with HIV.
Due to a combination of :
•economic decline,
•the breakdown of health systems,
•insufficient application of TB control measures,
•the spread of HIV/AIDS and
•the emergence of multidrug-resistant TB.
TB is on the rise in many developing and transitional economies
•Who are on most risk?
•Malnourished, The high number of imprisoned persons, Overcrowded
conditions, Inadequate ventilation, Elderly, and
Poor,migrants,smokers,other
comorbidities,Chronicalcoholics,HIV/AIDS,Silicosis,Increasing drug
resistance.
.
Control and prevention
TB control and prevention
Main strategies include:
BCG vaccination
Case finding
Effective chemotherapy
Health education
Chemoprophylaxis
In order to reverse the increasing trend in TB, effective control
and prevention is required in all countries
INTESTINAL INFECTIONS
 POLIOMYELITIS
 VIRAL HEPATITIS
 ADD
 CHOLERA
 TYPHOID
 FOOD POISONING
 AMOEBIASIS
 ASCARIASIS
 HOOKWORM INFECTION
 DRACUNCULIASIS
POLIOMYELITIS
Acute viral infection caused by an RNA virus.
Primarily an infection of the alimentary tract but the virus may spread
to CNS also in very small percentage of cases resulting in varying
degrees of paralysis and possibly death.
AGENT -Polio virus which belongs to the family picornaviridae.
Classified into three types-Type 1,2,3.
Type 1-most common and causes most epidemics.
Type2-usually causes endemic infection.
Type3-causes epidemics.
Reservoir of infection:Man is the only known source of infection.Most
of the infections are sub clinical.
Infectious Material- faeces and oropharyngeal secretions of infected
person.
- The half life of virus is 48 hrs in sewage and spread can occur during
this period
Host Factors:
• Age- mostly infancy and childhood.
• Sex-it has been noted in the ratio of 3males to one female.
• Immunity-immunity following infection is fairly solid although
reinfection can occur since infection with one type does not protect
completely against the other two type.
• Pregnancy
Environmental Factors:
• More likely during rainy season.
• Contaminated water,food,flies.
• Survives for a long time in a cold environment.
• Over crowding and poor sanitation
Period Of Communicability- cases are most infectious 7 to 10 days
before and after onset of symptoms.
In faeces,virus is excreted commonly for 2 to 3 weeks ,sometimes as
long as 3 to 4 months.
Mode Of Transmission
Faeco-oral route-this is the main route of transmission in developing
countries.
The infection may spread directly through contaminated fingers
where hygiene is poor or indirectly through contaminated
water,milk,foods,flies and articles of daily use.
Droplet infection-occurs in acute stage where virus is in throat.
Incubation Period –
It is usually 7 to 14 days (range 3 to 35 days)
Viral hepatitis
Defined as inflammation of the liver.
Viruses identified until now have been named as a,b c, d,e&g
Agent
Picornaviridae family
Resistance: the virus withstands heating to 60deg c for 1 hour.
Virus is inactivated by formalin,uvrays and by boiling for 5mins.Or
autoclaving.
Reservoir of infection:-human cases the only reservoir of infection.
Asymptomatic (anicteric)infections are especially common in
children.No evidence of chronic carrier state.
Period of infectivity:-2weeks before to 1week after the onset of
jaundice.
Infective material: faeces;blood,serum & other fluids-during brief
stage of viremia.
Virus excretion:hav excreted in faeces for about 2weeks before and
1week after onset of jaundice.
Incubation period- 15-45 days
Environmental factors:
In India associated with heavy rainfall.
Poor sanitation and overcrowding -water borne and food borne
epidemics.
Faeco-oral route: major route of transmission.
direct(person-to-person)contact or indirectly by contaminated
water,food or milk.
Food borne outbreaks (raw or inadequately cooked shellfish cultivated in
sewage polluted water)
Poor sanitation and overcrowding.
PARENTERAL
Hepatitis A rarely(blood and blood products/contaminated needles).
SEXUAL TRANSMISSION
This may occur mainly in homosexual men.
PRIMARY PREVENTION
HEALTH PROMOTION
The people must be educated about proper sanitation and good
personal hygiene (eg.washing oh hands after defaecation,before
preparing food,before eating etc)
Purification of community water supplies by flocculation,filtration
and adequate chlorination
Boiling water before drinking
SPECIFIC PROTECTION
This is means of a vaccine
Sometimes passively by immunoglobulins.
ACUTE DIARRHEAL DISEASE
Passing of liquid or watery stools atleast 3 times in a 24 hour period
.
Consistency rather than the number of stools
Acute :Sudden onset which lasts for 3-7days .
Chronic :Diarrhoea lasting 3 weeks or more.
Agent factors:Age : common in children between 6 months -2years.
Incidence highest in age group 6-11months when weaning occurs.
Nutrition ::: diarrhoea common in malnourished.
Socioeconomic factors:Poverty.
Incorrect feeding practices.
Prematurity.
Immunodeficiency.
Lack of personal and domestic hygeine.
Environmental factors:seasonal pattern in most developing
countries .
Cholera in winter.
Rotaviruses in winter
Shigella in dry summer
CHOLERA
An acute diarrhoeal disease.
Cause by vibrio cholerae.
A gram negative organism
5-10% of acute diarrhoeal cases.
Profuse painless watery diarrhoea.
Followed by vomiting, rapid dehydration and suppression of
urine.
Leading to hypovolemic shock & death in less than 24 hrs.
Cholera stool: colour less watery fluid with flecks of mucus.
Called as rice water stools.
Mode of transmission:Occurs from man to man.
3 routes :
1. Faecally contaminated
Water.
2. Contaminated food &
drinks.
3. Direct contact.
Agent factors:
Causative org : vibrio cholerae
Two sero groups – o1& non o1
Two biotypes - classical & eltor.
Each biotype – 3 sero types:
Susceptible to heat drying & acids.
Resistance:resist high alkalinity,30 min by boiling at 56 c.
Survival in water:grossly contaminated water - ganges donot survive
Clean water survive up to 30 days.
Survival in water influenced by ph,temp,salinity
Susceptible to common disinfectants - eltor more resistant.
Reservoir:human
Source of infection : cholera stools & vomit.
No.Of vibrios per ml of stool
1.Cases - 107 -109
2.Carriers - 102 -105
Pts excrete 10 – 20 lits of fluid.
Cholera is dose related.
Infective dose – 1011 orgs.
Infection :
ingestion of more than infective dose.
Case is infectious for 7-10 days.
Convalescent carrier infectious – 2 - 3 wks.
Chronic carrier – up to 10 yrs.
Chronic carriers less in classical more often in eltor.
TYPHOID
Severe, contagious,& life threatining disease.It is caused by
contaminated food, drinks & water by bacteria called S.Typhi, which
may result in fever with severe complications.
Agent:- major cause S.Typhi,S.Paratyhpi a & b
S.Typhi:- gram -ve, motile, peritrichate flagella .It has three main
antigens o ,h ,vi.
It was readily killed by drying,pasteurisation & common disinfectants.
Man is a only reservoir of infection {cases & carriers }
Carriers :temporary –the patient who shed bacilli >3months.
Chronic - >1year.
Convalescent- 3weeks - 3months.
Source of infection:Primary source:- faeces & urine of cases & carriers.
Secondary source:-contaminated water ,food,finger & nails.
No evidence of typhoid bacilli excreted in sputum & milk.
Social and environmental factors:Peak of incidence:-july &
september.This period coincides with rainy season & an increase fly
population.
Social factors:-pollution of drinking water supplies, open air
defecation & urination, low standards of food & personal hygeine &
health ignorance,vegetables grown in sewage forms contaminated with
water.
IP:10 – 14 days.But it may be as short as 3 days or as long as 3 weeks
depending upon of the dose of bacilli ingested.
Modes of transmission:-faeco-oral route.Ingestion of contaminated
water, milk & food.
FOOD POISONING
Acute gastro - enteritis caused by ingestion of food or drink
contaminated by
Living bacteria
Bacterial toxins
Inorganic chemical substances
Poisons– plants and animals
It is a point source epidemic-
H/o of consumption of same food.
Same symptoms in group of people.
Attack of same persons at same time.
Caused by following bacteria
Bacterial poisoning:
Infective and toxic types
Caused by following bacteria
• Salmonella
• Staphylococcus
• Botulism (cl.Botulinum)
• Cl.Perfringens
• B.Cereus
Investigation of food poisoning
Secure people list of involved and their history.
! Foods eaten during previous two days
! Symptoms- time of onset, type
! Personal data
Laboratory investigations.
! Isolation of causative organism- stool,vomit, remnant food
! Stool samples of kitchen employees
Prevention and control
AMEOBIASIS
Agent:E.Histolytica
Reservoir:Man is the only reservoir of infection.
The intermediate source of infection is the faeces containing the cysts.
Most individuals infected with E.histolytica remain symptom free and
are healthy carriers of the parasite.
The carrier can discharge up to 1.5 x 107 cysts daily.
Period of communicability :
As long as cysts are excreted; the period may be several years, if carriers
are unrecognized and untreated.
Mode of transmission:Faeco-oral route
This may readily take place through intake of contaminated water or
food.
Vegetables especially those eaten raw, from fields irrigated with sewage
polluted water can rapidly convey infection.
Viable cysts are found on the hands and under finger nails. This may lead
to direct hand to mouth transmission.
ASCARIASIS
Most common helminthic infestation.
Ascariasis is found worldwide. More than 1.4 billion people are
infected.
Prevalence of infestation during 1997 was 250 million
Severe ascaris infections cause approx. 60,000 deaths per year,
mostly children
Agent :Ascaris Lumbricoides
Reservoir of infection : man
Infective material:
feces containing Fertilized eggs
Ascaris eggs are more likely to survive, and develop more rapidly, in
shady, moist, clay soil
Single female lays about 2 lack eggs per day.
Mode Of Infection:
Faecal-oral Route– Ingestion Of Food And Water Contaminated With
Eggs.
Eating Uncooked Food Grown In Contaminated Soil.
Fingers Contaminated With Soil.
Incubation Period: About 2 Months.
HOOK WORM
ARTHROPOD BORNE DISEASES
DENGUE SYNDROME
Spread by a bite of infected mosquitoes.
Flavivirus (Dengue 1,2,3,4).
Dengue virus manifests as:
Dengue Fever: Flu like illness
Dengue Hemorrhagic Fever: Severe often fatal
Resevoir of infection
Man is the main reservoir of virus.
Monkey is the jungle reservoir in Malaysia and
Africa.
Host: Human
Sex: Both
Age: All Age groups
Mode of transmission:
human to human by mosquito bite.
Vector:AEDES AEGYPTI- A polynesiensis, A sentellaris, A
pseudosentellaris, A albopictus are the vectors.
Female mosquitoes bites human during the day.
Incubation period: 3-10 days (commonly 5-6 days).
An infected person can’t spread the infectious to others but can
be a source of dengue virus for mosquitoes for 6 days.
Environmental factors:
Breed in discarded types flower pots, old oil drums, water
storage containers.
Aedes breed in artificial collections of water
LYMPHATIC FILARIASIS
Worldwide prevalent, arthropod borne,
causing
permanent, long term disability &
disfigurement &
associated with social & economic
stigma.
It causes-Isolation
-Psychological stress
-Family discord
-Impair employment
-Impair mobility & activities
AGENTS
• W.BANCROFTI
• B.MALAYI
• B.TIMORI
• Definite host is MAN.
• Intermediate host is MOSQUITO.
• Adult worms live in LYMPHATIC SYSTEM remain coiled
together.
• Male 2.5-4cm. & Female 8-10cm.
• Mf are seen in blood, lung (capillaries), kidney,(glomerular
tufts).
Adult female worm gives birth to as many as 50,000 Mf/day
(VIVIPAROUS)
Enter the blood via lymphatics
During blood meal, enter into mosquito
Within 15-30 min.exsheathing in stomach
Penetrate stomach wall & enter thoracic muscles
Develop into first,sec,third stages
Third stage migrate to the proboscis of mosq(infective)
Through bite they enter humans
Reservoirs-HUMANS - is a person with circulating Mf in peripheral
blood.
Host Factors
MAN is a natural host.
All ages are susceptible.
Sex :higher in men.
Migration: causes extension of filariasis into areas previously non
endemic.
Immunity: resistance to infection after many years of exposure.
Environmental Factors
A) Climate: 1)Mosquito-longevity & breeding
2)determines the development of parasite in the vector
B) Town planning: rapid urbanization in INDIA -inadequate sewage
disposal
C) Drainage: breed profusely in polluted water.
Common breeding habits
1)culex-cess pools, soakage pits, ill maintained drains, septic tanks,
open ditches, burrow pits,etc.
2)mansonia-confined to areas where pistia plants are there.
MALARIA
1.1 -- 2.7 million people are killed by this disease worldwide, each
year.
Host factors
Age: Mostly all ages.
Sex: Males at greater risk
Race: Sickle cell trait -- Milder illness with P. falciparum
Duffy –ve RBC -- Resistant to P. vivax
Pregnancy: Primigravidae,IUD, premature labor or abortion
Socio-economic development: Low
Housing:
ill ventilated & ill lighted ( indoor resting places)
site, type of construction influence selection of control measures
Population mobility:
Internal migration
Imported malaria [ Europe, N.America & temperate parts of
the world ]
Occupation: Mostly agrarian [rural backdrop]
Human habits:
Sleeping outdoors
Nomads
Refusal to accept spraying of houses
Not using methods of personal protection like bed nets etc.
Immunity:
Collective immunity comes into play
Immune mothers -- infants protected 3-5 months by maternal
IgG
Semi immune -- partially protected
Active immunity is species specific
Humoral and cellular responses help in protection
Mode of transmission
Vector transmission : Female Anopheline mosquitoes
Direct transmission : Accidentally by hypodermic i.m & i.v
injections of blood or plasma
Congenital transmission : Rare
Incubation period
Usually not less than 10 days
Varies with species
P. falciparum malaria – 12 days [9-14 ]
P. vivax – 14 days [8-17]
Quartan malaria – 28 days [ 18-40]
P. ovale – 17 days [16-18]
Clinical features
Fever with characteristic paroxysms
Typical attack comprises of three distinct stages:
Cold stage
Severe headache, chilly sensation, vomiting
Parasites demonstrable in blood
Lasts for ¼ --1 hr
Hot stage
Burning sensation
Hot skin and dry to touch
Rapid respiration
Lasts for 2 –6 hrs.
Sweating stage
Profuse sweating with fall in temp.
Lasts for 2– 4 hrs
Followed by an afebrile period – patient feels greatly relieved
epidemiology of common infectious diseases-resp,git,arthropod.pptx

More Related Content

Similar to epidemiology of common infectious diseases-resp,git,arthropod.pptx

Common Pediatric Viral Exanthems
Common Pediatric Viral Exanthems Common Pediatric Viral Exanthems
Common Pediatric Viral Exanthems Fatima Farid
 
Bioterrorism
BioterrorismBioterrorism
Bioterrorismdrguru007
 
Influenza, Bird Flu, SARS & Swine Flu.pptx
Influenza, Bird Flu, SARS & Swine Flu.pptxInfluenza, Bird Flu, SARS & Swine Flu.pptx
Influenza, Bird Flu, SARS & Swine Flu.pptxRahul Netragaonkar
 
EPIDEMIOLOGY – COMMUNICABLE DISEASE.pptx
EPIDEMIOLOGY – COMMUNICABLE DISEASE.pptxEPIDEMIOLOGY – COMMUNICABLE DISEASE.pptx
EPIDEMIOLOGY – COMMUNICABLE DISEASE.pptxNiranjani sakthivel
 
monkeypox- amended 2.pptx
monkeypox- amended 2.pptxmonkeypox- amended 2.pptx
monkeypox- amended 2.pptxHelen Utaji
 
MEASLES.pptx4445544444444444444444444444
MEASLES.pptx4445544444444444444444444444MEASLES.pptx4445544444444444444444444444
MEASLES.pptx4445544444444444444444444444samuellamaryk
 
Chickenpox Varicella zoster virus.VZV FIJI
Chickenpox Varicella zoster virus.VZV FIJIChickenpox Varicella zoster virus.VZV FIJI
Chickenpox Varicella zoster virus.VZV FIJIOsamaBinKhalid2
 
MEASLES - THEORY.ppt
MEASLES - THEORY.pptMEASLES - THEORY.ppt
MEASLES - THEORY.pptmousaderhem1
 
Epidemiology and nursing management for mumps- CHN.pptx
Epidemiology and nursing management for mumps- CHN.pptxEpidemiology and nursing management for mumps- CHN.pptx
Epidemiology and nursing management for mumps- CHN.pptxAngel480700
 
Measles .pptx
Measles .pptxMeasles .pptx
Measles .pptxBeema3
 
Measles .pptx
Measles .pptxMeasles .pptx
Measles .pptxBeema3
 
MSN I COMMUNICABLE DISEASES.pptx
MSN I COMMUNICABLE DISEASES.pptxMSN I COMMUNICABLE DISEASES.pptx
MSN I COMMUNICABLE DISEASES.pptx M.Josephin Dayana
 
Fever and rash by Dr.Uma
Fever and rash by Dr.UmaFever and rash by Dr.Uma
Fever and rash by Dr.UmaDr. Rubz
 

Similar to epidemiology of common infectious diseases-resp,git,arthropod.pptx (20)

Common Pediatric Viral Exanthems
Common Pediatric Viral Exanthems Common Pediatric Viral Exanthems
Common Pediatric Viral Exanthems
 
Bioterrorism
BioterrorismBioterrorism
Bioterrorism
 
Influenza, Bird Flu, SARS & Swine Flu.pptx
Influenza, Bird Flu, SARS & Swine Flu.pptxInfluenza, Bird Flu, SARS & Swine Flu.pptx
Influenza, Bird Flu, SARS & Swine Flu.pptx
 
EPIDEMIOLOGY – COMMUNICABLE DISEASE.pptx
EPIDEMIOLOGY – COMMUNICABLE DISEASE.pptxEPIDEMIOLOGY – COMMUNICABLE DISEASE.pptx
EPIDEMIOLOGY – COMMUNICABLE DISEASE.pptx
 
monkeypox- amended 2.pptx
monkeypox- amended 2.pptxmonkeypox- amended 2.pptx
monkeypox- amended 2.pptx
 
MEASLES.pptx4445544444444444444444444444
MEASLES.pptx4445544444444444444444444444MEASLES.pptx4445544444444444444444444444
MEASLES.pptx4445544444444444444444444444
 
Chickenpox Varicella zoster virus.VZV FIJI
Chickenpox Varicella zoster virus.VZV FIJIChickenpox Varicella zoster virus.VZV FIJI
Chickenpox Varicella zoster virus.VZV FIJI
 
Airborrne and vectorborne
Airborrne and vectorborneAirborrne and vectorborne
Airborrne and vectorborne
 
Airborrne and vectorborne
Airborrne and vectorborneAirborrne and vectorborne
Airborrne and vectorborne
 
vaccine pre1.pptx
vaccine pre1.pptxvaccine pre1.pptx
vaccine pre1.pptx
 
MEASLES - THEORY.ppt
MEASLES - THEORY.pptMEASLES - THEORY.ppt
MEASLES - THEORY.ppt
 
Mumps & Rubella.pptx
Mumps & Rubella.pptxMumps & Rubella.pptx
Mumps & Rubella.pptx
 
Epidemiology and nursing management for mumps- CHN.pptx
Epidemiology and nursing management for mumps- CHN.pptxEpidemiology and nursing management for mumps- CHN.pptx
Epidemiology and nursing management for mumps- CHN.pptx
 
Measles .pptx
Measles .pptxMeasles .pptx
Measles .pptx
 
Measles .pptx
Measles .pptxMeasles .pptx
Measles .pptx
 
Measles
MeaslesMeasles
Measles
 
Chickenpox
ChickenpoxChickenpox
Chickenpox
 
MSN I COMMUNICABLE DISEASES.pptx
MSN I COMMUNICABLE DISEASES.pptxMSN I COMMUNICABLE DISEASES.pptx
MSN I COMMUNICABLE DISEASES.pptx
 
COMMUNIABLE DISEASE.pptx
COMMUNIABLE DISEASE.pptxCOMMUNIABLE DISEASE.pptx
COMMUNIABLE DISEASE.pptx
 
Fever and rash by Dr.Uma
Fever and rash by Dr.UmaFever and rash by Dr.Uma
Fever and rash by Dr.Uma
 

More from sanakhader3

C03 P03 MEASEUREMENT OF MORBIDITY.ppt
C03 P03 MEASEUREMENT OF MORBIDITY.pptC03 P03 MEASEUREMENT OF MORBIDITY.ppt
C03 P03 MEASEUREMENT OF MORBIDITY.pptsanakhader3
 
nutrition sources.pptx
nutrition sources.pptxnutrition sources.pptx
nutrition sources.pptxsanakhader3
 
C04 P02 CRITERIA FOR SCREENING TESTS.ppt
C04 P02 CRITERIA FOR SCREENING TESTS.pptC04 P02 CRITERIA FOR SCREENING TESTS.ppt
C04 P02 CRITERIA FOR SCREENING TESTS.pptsanakhader3
 
measures of central tendency.pptx
measures of central tendency.pptxmeasures of central tendency.pptx
measures of central tendency.pptxsanakhader3
 
JSS MC-PG- IMR PREVENTION.ppt
JSS MC-PG- IMR PREVENTION.pptJSS MC-PG- IMR PREVENTION.ppt
JSS MC-PG- IMR PREVENTION.pptsanakhader3
 
MATERNAL MORTALITY CAUSES.ppt
MATERNAL MORTALITY CAUSES.pptMATERNAL MORTALITY CAUSES.ppt
MATERNAL MORTALITY CAUSES.pptsanakhader3
 

More from sanakhader3 (7)

C03 P03 MEASEUREMENT OF MORBIDITY.ppt
C03 P03 MEASEUREMENT OF MORBIDITY.pptC03 P03 MEASEUREMENT OF MORBIDITY.ppt
C03 P03 MEASEUREMENT OF MORBIDITY.ppt
 
nutrition sources.pptx
nutrition sources.pptxnutrition sources.pptx
nutrition sources.pptx
 
news.pptx
news.pptxnews.pptx
news.pptx
 
C04 P02 CRITERIA FOR SCREENING TESTS.ppt
C04 P02 CRITERIA FOR SCREENING TESTS.pptC04 P02 CRITERIA FOR SCREENING TESTS.ppt
C04 P02 CRITERIA FOR SCREENING TESTS.ppt
 
measures of central tendency.pptx
measures of central tendency.pptxmeasures of central tendency.pptx
measures of central tendency.pptx
 
JSS MC-PG- IMR PREVENTION.ppt
JSS MC-PG- IMR PREVENTION.pptJSS MC-PG- IMR PREVENTION.ppt
JSS MC-PG- IMR PREVENTION.ppt
 
MATERNAL MORTALITY CAUSES.ppt
MATERNAL MORTALITY CAUSES.pptMATERNAL MORTALITY CAUSES.ppt
MATERNAL MORTALITY CAUSES.ppt
 

Recently uploaded

Cell structure slideshare.pptx Unlocking the Secrets of Cells: Structure, Fun...
Cell structure slideshare.pptx Unlocking the Secrets of Cells: Structure, Fun...Cell structure slideshare.pptx Unlocking the Secrets of Cells: Structure, Fun...
Cell structure slideshare.pptx Unlocking the Secrets of Cells: Structure, Fun...ananyagirishbabu1
 
Valle Egypt Illustrates Consequences of Financial Elder Abuse
Valle Egypt Illustrates Consequences of Financial Elder AbuseValle Egypt Illustrates Consequences of Financial Elder Abuse
Valle Egypt Illustrates Consequences of Financial Elder AbuseKristin Hetzer
 
Virtual Health Platforms_ Revolutionizing Patient Care.pdf
Virtual Health Platforms_ Revolutionizing Patient Care.pdfVirtual Health Platforms_ Revolutionizing Patient Care.pdf
Virtual Health Platforms_ Revolutionizing Patient Care.pdfsmartcare
 
QA Paediatric dentistry department, Hospital Melaka 2020
QA Paediatric dentistry department, Hospital Melaka 2020QA Paediatric dentistry department, Hospital Melaka 2020
QA Paediatric dentistry department, Hospital Melaka 2020Azreen Aj
 
GENERAL PHARMACOLOGY - INTRODUCTION DENTAL.ppt
GENERAL PHARMACOLOGY - INTRODUCTION DENTAL.pptGENERAL PHARMACOLOGY - INTRODUCTION DENTAL.ppt
GENERAL PHARMACOLOGY - INTRODUCTION DENTAL.pptMangaiarkkarasi
 
💃Joint ❤89011-83002❤ #ℂALL #gIRLS Ludhiana Escorts by ✔️🍑💃Hotel #cALL #gIRLS...
💃Joint ❤89011-83002❤ #ℂALL #gIRLS Ludhiana Escorts  by ✔️🍑💃Hotel #cALL #gIRLS...💃Joint ❤89011-83002❤ #ℂALL #gIRLS Ludhiana Escorts  by ✔️🍑💃Hotel #cALL #gIRLS...
💃Joint ❤89011-83002❤ #ℂALL #gIRLS Ludhiana Escorts by ✔️🍑💃Hotel #cALL #gIRLS...aunty1x1
 
PhRMA Vaccines Deck_05-15_2024_FINAL.pptx
PhRMA Vaccines Deck_05-15_2024_FINAL.pptxPhRMA Vaccines Deck_05-15_2024_FINAL.pptx
PhRMA Vaccines Deck_05-15_2024_FINAL.pptxBlake100757
 
#cALL# #gIRLS# In Chhattisgarh ꧁❤8901183002❤꧂#cALL# #gIRLS# Service In Chhatt...
#cALL# #gIRLS# In Chhattisgarh ꧁❤8901183002❤꧂#cALL# #gIRLS# Service In Chhatt...#cALL# #gIRLS# In Chhattisgarh ꧁❤8901183002❤꧂#cALL# #gIRLS# Service In Chhatt...
#cALL# #gIRLS# In Chhattisgarh ꧁❤8901183002❤꧂#cALL# #gIRLS# Service In Chhatt...aunty1x1
 
R3 Stem Cells and Kidney Repair A New Horizon in Nephrology.pptx
R3 Stem Cells and Kidney Repair A New Horizon in Nephrology.pptxR3 Stem Cells and Kidney Repair A New Horizon in Nephrology.pptx
R3 Stem Cells and Kidney Repair A New Horizon in Nephrology.pptxR3 Stem Cell
 
Occupational Therapy Management for Parkinson's Disease - Webinar 2024
Occupational Therapy Management for Parkinson's Disease - Webinar 2024Occupational Therapy Management for Parkinson's Disease - Webinar 2024
Occupational Therapy Management for Parkinson's Disease - Webinar 2024Phinoj K Abraham
 
pathology seminar presentation best ppt by .pptx
pathology seminar presentation best ppt by  .pptxpathology seminar presentation best ppt by  .pptx
pathology seminar presentation best ppt by .pptxAmanuelIbrahim
 
Breaking Down Oppositional Defiant Disorder Treatments
Breaking Down Oppositional Defiant Disorder TreatmentsBreaking Down Oppositional Defiant Disorder Treatments
Breaking Down Oppositional Defiant Disorder TreatmentsOppositional Defiant Disorder
 
Jesse Jhaj: Building Relationships with Patients as a Doctor or Healthcare Wo...
Jesse Jhaj: Building Relationships with Patients as a Doctor or Healthcare Wo...Jesse Jhaj: Building Relationships with Patients as a Doctor or Healthcare Wo...
Jesse Jhaj: Building Relationships with Patients as a Doctor or Healthcare Wo...saimasadaf14
 
Demystifying-Gene-Editing-The-Promise-and-Peril-of-CRISPR.pdf
Demystifying-Gene-Editing-The-Promise-and-Peril-of-CRISPR.pdfDemystifying-Gene-Editing-The-Promise-and-Peril-of-CRISPR.pdf
Demystifying-Gene-Editing-The-Promise-and-Peril-of-CRISPR.pdfSasikiranMarri
 
Nose-Nasal Cavity & Paranasal Sinuses BY Dr.Rabia Inam Gandapore.pptx
Nose-Nasal Cavity & Paranasal Sinuses BY Dr.Rabia Inam Gandapore.pptxNose-Nasal Cavity & Paranasal Sinuses BY Dr.Rabia Inam Gandapore.pptx
Nose-Nasal Cavity & Paranasal Sinuses BY Dr.Rabia Inam Gandapore.pptxDr. Rabia Inam Gandapore
 
Importance of Diet on Dental Health.docx
Importance of Diet on Dental Health.docxImportance of Diet on Dental Health.docx
Importance of Diet on Dental Health.docxSachin Mittal
 
Healthcare Companion Robots: Key Features and Functionalities, Benefits, Chal...
Healthcare Companion Robots: Key Features and Functionalities, Benefits, Chal...Healthcare Companion Robots: Key Features and Functionalities, Benefits, Chal...
Healthcare Companion Robots: Key Features and Functionalities, Benefits, Chal...GQ Research
 
The Docs PPG - 30.01.2024.pptx..........
The Docs PPG - 30.01.2024.pptx..........The Docs PPG - 30.01.2024.pptx..........
The Docs PPG - 30.01.2024.pptx..........TheDocs
 
Dehradun ❤CALL Girls 8901183002 ❤ℂall Girls IN Dehradun ESCORT SERVICE❤
Dehradun ❤CALL Girls  8901183002 ❤ℂall  Girls IN Dehradun ESCORT SERVICE❤Dehradun ❤CALL Girls  8901183002 ❤ℂall  Girls IN Dehradun ESCORT SERVICE❤
Dehradun ❤CALL Girls 8901183002 ❤ℂall Girls IN Dehradun ESCORT SERVICE❤aunty1x2
 
Jaipur #ℂall #gIRLS Oyo Hotel 89O1183OO2 #ℂall #gIRL in Jaipur
Jaipur #ℂall #gIRLS Oyo Hotel 89O1183OO2 #ℂall #gIRL in Jaipur Jaipur #ℂall #gIRLS Oyo Hotel 89O1183OO2 #ℂall #gIRL in Jaipur
Jaipur #ℂall #gIRLS Oyo Hotel 89O1183OO2 #ℂall #gIRL in Jaipur aunty1x1
 

Recently uploaded (20)

Cell structure slideshare.pptx Unlocking the Secrets of Cells: Structure, Fun...
Cell structure slideshare.pptx Unlocking the Secrets of Cells: Structure, Fun...Cell structure slideshare.pptx Unlocking the Secrets of Cells: Structure, Fun...
Cell structure slideshare.pptx Unlocking the Secrets of Cells: Structure, Fun...
 
Valle Egypt Illustrates Consequences of Financial Elder Abuse
Valle Egypt Illustrates Consequences of Financial Elder AbuseValle Egypt Illustrates Consequences of Financial Elder Abuse
Valle Egypt Illustrates Consequences of Financial Elder Abuse
 
Virtual Health Platforms_ Revolutionizing Patient Care.pdf
Virtual Health Platforms_ Revolutionizing Patient Care.pdfVirtual Health Platforms_ Revolutionizing Patient Care.pdf
Virtual Health Platforms_ Revolutionizing Patient Care.pdf
 
QA Paediatric dentistry department, Hospital Melaka 2020
QA Paediatric dentistry department, Hospital Melaka 2020QA Paediatric dentistry department, Hospital Melaka 2020
QA Paediatric dentistry department, Hospital Melaka 2020
 
GENERAL PHARMACOLOGY - INTRODUCTION DENTAL.ppt
GENERAL PHARMACOLOGY - INTRODUCTION DENTAL.pptGENERAL PHARMACOLOGY - INTRODUCTION DENTAL.ppt
GENERAL PHARMACOLOGY - INTRODUCTION DENTAL.ppt
 
💃Joint ❤89011-83002❤ #ℂALL #gIRLS Ludhiana Escorts by ✔️🍑💃Hotel #cALL #gIRLS...
💃Joint ❤89011-83002❤ #ℂALL #gIRLS Ludhiana Escorts  by ✔️🍑💃Hotel #cALL #gIRLS...💃Joint ❤89011-83002❤ #ℂALL #gIRLS Ludhiana Escorts  by ✔️🍑💃Hotel #cALL #gIRLS...
💃Joint ❤89011-83002❤ #ℂALL #gIRLS Ludhiana Escorts by ✔️🍑💃Hotel #cALL #gIRLS...
 
PhRMA Vaccines Deck_05-15_2024_FINAL.pptx
PhRMA Vaccines Deck_05-15_2024_FINAL.pptxPhRMA Vaccines Deck_05-15_2024_FINAL.pptx
PhRMA Vaccines Deck_05-15_2024_FINAL.pptx
 
#cALL# #gIRLS# In Chhattisgarh ꧁❤8901183002❤꧂#cALL# #gIRLS# Service In Chhatt...
#cALL# #gIRLS# In Chhattisgarh ꧁❤8901183002❤꧂#cALL# #gIRLS# Service In Chhatt...#cALL# #gIRLS# In Chhattisgarh ꧁❤8901183002❤꧂#cALL# #gIRLS# Service In Chhatt...
#cALL# #gIRLS# In Chhattisgarh ꧁❤8901183002❤꧂#cALL# #gIRLS# Service In Chhatt...
 
R3 Stem Cells and Kidney Repair A New Horizon in Nephrology.pptx
R3 Stem Cells and Kidney Repair A New Horizon in Nephrology.pptxR3 Stem Cells and Kidney Repair A New Horizon in Nephrology.pptx
R3 Stem Cells and Kidney Repair A New Horizon in Nephrology.pptx
 
Occupational Therapy Management for Parkinson's Disease - Webinar 2024
Occupational Therapy Management for Parkinson's Disease - Webinar 2024Occupational Therapy Management for Parkinson's Disease - Webinar 2024
Occupational Therapy Management for Parkinson's Disease - Webinar 2024
 
pathology seminar presentation best ppt by .pptx
pathology seminar presentation best ppt by  .pptxpathology seminar presentation best ppt by  .pptx
pathology seminar presentation best ppt by .pptx
 
Breaking Down Oppositional Defiant Disorder Treatments
Breaking Down Oppositional Defiant Disorder TreatmentsBreaking Down Oppositional Defiant Disorder Treatments
Breaking Down Oppositional Defiant Disorder Treatments
 
Jesse Jhaj: Building Relationships with Patients as a Doctor or Healthcare Wo...
Jesse Jhaj: Building Relationships with Patients as a Doctor or Healthcare Wo...Jesse Jhaj: Building Relationships with Patients as a Doctor or Healthcare Wo...
Jesse Jhaj: Building Relationships with Patients as a Doctor or Healthcare Wo...
 
Demystifying-Gene-Editing-The-Promise-and-Peril-of-CRISPR.pdf
Demystifying-Gene-Editing-The-Promise-and-Peril-of-CRISPR.pdfDemystifying-Gene-Editing-The-Promise-and-Peril-of-CRISPR.pdf
Demystifying-Gene-Editing-The-Promise-and-Peril-of-CRISPR.pdf
 
Nose-Nasal Cavity & Paranasal Sinuses BY Dr.Rabia Inam Gandapore.pptx
Nose-Nasal Cavity & Paranasal Sinuses BY Dr.Rabia Inam Gandapore.pptxNose-Nasal Cavity & Paranasal Sinuses BY Dr.Rabia Inam Gandapore.pptx
Nose-Nasal Cavity & Paranasal Sinuses BY Dr.Rabia Inam Gandapore.pptx
 
Importance of Diet on Dental Health.docx
Importance of Diet on Dental Health.docxImportance of Diet on Dental Health.docx
Importance of Diet on Dental Health.docx
 
Healthcare Companion Robots: Key Features and Functionalities, Benefits, Chal...
Healthcare Companion Robots: Key Features and Functionalities, Benefits, Chal...Healthcare Companion Robots: Key Features and Functionalities, Benefits, Chal...
Healthcare Companion Robots: Key Features and Functionalities, Benefits, Chal...
 
The Docs PPG - 30.01.2024.pptx..........
The Docs PPG - 30.01.2024.pptx..........The Docs PPG - 30.01.2024.pptx..........
The Docs PPG - 30.01.2024.pptx..........
 
Dehradun ❤CALL Girls 8901183002 ❤ℂall Girls IN Dehradun ESCORT SERVICE❤
Dehradun ❤CALL Girls  8901183002 ❤ℂall  Girls IN Dehradun ESCORT SERVICE❤Dehradun ❤CALL Girls  8901183002 ❤ℂall  Girls IN Dehradun ESCORT SERVICE❤
Dehradun ❤CALL Girls 8901183002 ❤ℂall Girls IN Dehradun ESCORT SERVICE❤
 
Jaipur #ℂall #gIRLS Oyo Hotel 89O1183OO2 #ℂall #gIRL in Jaipur
Jaipur #ℂall #gIRLS Oyo Hotel 89O1183OO2 #ℂall #gIRL in Jaipur Jaipur #ℂall #gIRLS Oyo Hotel 89O1183OO2 #ℂall #gIRL in Jaipur
Jaipur #ℂall #gIRLS Oyo Hotel 89O1183OO2 #ℂall #gIRL in Jaipur
 

epidemiology of common infectious diseases-resp,git,arthropod.pptx

  • 1. Epidemiology of common infectious diseases This Photo by Unknown Author is licensed under CC BY-SA-NC
  • 2. RESPIRATORY INFECTIONS • SMALL POX • HUMAN MONKEYPOX • CHIKENPOX • MEASLES • RUBELLA • MUMPS • INFLUENZA • DIPHTERIA • PERTUSIS • ARI • COVID 19 • TUBERCULOSIS
  • 3.
  • 4. SMALL POX Caused by variola virus Acute onset of fever,headache,back ache, vomiting Rash on day 3 – centrifugal distribution Macule – papule – vesicle – pustule – scab – scarring Eradicated on 1977 ; last case in India 1977
  • 5. HUMAN MONKEY POX viral zoonosis Genus orthopoxvirus Natural hosts – squirrels , rodents , non human primates etc Transmission : Animal to human Direct contact with blood ,body fluids of infected animals. Eating animal products of infected animals Human to human: droplet infection , skin lesions
  • 6.
  • 7. Incubation period : 5 to 21 days Clinical picture : Fever, head ache, lymphadenopathy ,myalgia Rash on 3rd day – more on face and extremities Self limited disease Diagnosis : PCR (vesicle fluids/dry crusts) Management : symptomatic treatment , managing complications, preventing long term sequels. Prevention : awareness of risk factors health education Complications : secondary infections , bronchopneumonia ,sepsis, encephalitis , corneal infection.
  • 8. CHICKENPOX • Agent : varicella zoster virus/human alpha herpes virus 3 • Primary infection cause chickenpox • Recovery followed by latent infection. • Reactivation results in zoster- a painful, vesicular, pustular eruption in distribution of one or more sensory nerve roots. Incubation Period: Usually 14-16 days, although extremes as wide as 7-21 days have been reported. Transmission :Droplet infection and droplet nuclei. “Face to face” (personal) contact. Portal Of Entry: Respiratory tract.
  • 9. rash Eruptive Stage: Symmetrical. Appears on the trunk and then comes to face, arms ,legs. Mucosal surfaces (buccal, pharyngeal) are generally involved. Axilla may be affected. Palms and soles usually not involved. The density of eruption diminishes centrifugally. Rapid evolution: Stages of-macule - papule - vesicle - scab. Dew drops appearance of vesicles. Superficial in site, with easily ruptured walls and surrounded by inflammation. • Vesicles form crusts • Scabbing begins 4-7 days after the rash appears.
  • 10.
  • 11. CONTROL: No specific treatment for chicken pox. Notification. Isolation of cases for about 6 days after onset of rash. Disinfection of articles soiled by nose and throat discharges. VARICELLA ZOSTER IMMUNOGLOBULIN(VZIG): VZIG given within 72 hours of exposure has been recommended for prevention. DOSAGE:1.25-5ml intramuscularly.
  • 12. MEASLES • Measles is a highly contagious, acute, exanthemata's respiratory disease, with characteristic clinical picture and pathognomonic exanthem “koplik’s spots • Clinically characterized by fever and catarrhal symptoms of upper respiratory tract (coryza, cough), followed by typical rash.
  • 13. Epidemiological factors: AGENT: • RNA ParamyxoViruses. • Only one serotype known. • Cellular receptors for measles virus are CD46,CD156 expressed on Human lymphocytes. Genus: MORBILLI Family: Paramyxoviridae • Measles virus in droplet nuclei invade respiratory epithelium and attack reticuloendothelial system. SOURCE OF INFECTION: • Only case of measles • No carriers • No sub-clinical infections
  • 14. Infective material • Secretions from nose, throat and respiratory tract during prodromal period and early stages of rash. COMMUNICABILITY Highly infectious during prodromal period and at the time of eruption. Period of communicability: 4 days before the onset of rash to 5 days after the appearance of rash. Secondary attack rate: depends on susceptible children.
  • 15.  Host Factors  NUTRITION:Mortality due to measles in malnourished child is 400 times more than in well nourished cases.  Malnourished children excrete the virus for prolonged periods. So they are dangerous to the community. ENVIRONMENTAL:WINTER disease. India- winter and early spring. (i.e. Jan-April.) SOCIOECONOMIC FACTORS: poverty-malnutrition-low cell mediated immunity-prone to severe measles-increased mortality IMMUNITY: One attack gives lifelong immunity. Second attacks rare. Infants protected by maternal antibodies up to 6 months. Vaccination gives lifelong immunity.
  • 16. Transmission Direct Droplet infection. Droplet nuclei. Portal of entry: Respiratory tract Infection through conjunctiva also seen  Virus remains active and contagious in air or infected surface for up to 2 hr.  Recipients of vaccine are not contagious to others. Incubation Period 10 days from exposure to onset of fever and 14 days to appearance of rash.
  • 17. RUBELLA • Toga virus • RNA virus • Rapidly inactivated by chemicals light, low Ph, heat. • Reservoir: Human • Transmission:Respiratory,Subclinicalcases Communicability:7 days before and to 5-7 days after rash. Infants with CRS may shed virus for a year or more. • Incubation period 14 days(range 12-23 days) • Prodrome of low - grade fever • Lymphadenopathy in second week. • Maculo-papular rash 14-17 days after exposure.
  • 18. • Congenital rubella syndrome : hearing impairment congenital heart defect cataract • Rubella vaccine: Live viral vaccine RA 27/3 • Indications: All infants 12 months of age and older. • Susceptible adolescents and adults without documented evidence of rubella immunity. • Emphasis on nonpregnant women of childbearing age, particularly those born outside the U.S.
  • 19. MUMPS Mumps is an acute infectious disease caused by a virus which has a predilection for glandular and nervous tissue. EPIDEMIOLOGY Agent factors: Myxovirus parotidis Source:clinical and subclinical cases Period of communicability:4-6 days before symptoms and a week thereafter. Secondary attack rate :86% Host factors: 5-15 years More severe in adults One attack confers lifelong immunity i Environmental factors Endemic Peak in winter and spring overcrowding Mode of transmission:droplet infection IP:2 to 3 weeks(18days)
  • 20. Clinical features : pain and swelling of one or both parotid glands fever earache pain or stiffness on opening mouth swelling subsides over 1-2 weeks complications : orchitis , oophoritis , encephalopathy
  • 21. INFLUENZA Acute respiratory infection caused by influenza A,B,C,D viruses Sudden onset of malaise,chills,fever,muscle pain,cough 1918 Spanish influenza 1957 Asian influenza 1968 Hong Kong influenza 2009 Swine flu/H1N1 Presently circulating – A(H1N1),A(H3N2),B(H3N2) •The virus is spreading rapidly reaching all continents less than 3 months due to the speed of international air travel today.
  • 22. •Epidemiologic determinants AGENT: Family Orthomyxoviridae There are 3 types : Type A Type B Type C Antigenically distinct No cross immunity Reservoir of infection:Mainly - Animals & Birds Some include H and N antigens related to humans New strains by recombination influenza virus between man animals birds.
  • 23. •Host Factors:Usually case are subclicinal case. Nasal secretions are infective. • During epidemics,large number of mild and Asympomatic occurs play an important role in spread of infection. (A) Age and Sex: All ages and both sexes Highest mortality rate amount certain high risks groups. Example: Old people children under 18 months ,diabetes, or CHD. (B) Human Mobility : Important factors in spread of infection.
  • 24. (C) Immunity : Subtype specific Antibodies against HAAND NA Antibodies appear about 7 days after the attack and reach maximum level in about 2 weeks after 8 to 12 months,level drops to pre infection level. (D)Environmental factors: Season overcrowding
  • 25. Mode of transmission: Persons to persons by droplet infection or nuclei created by sneezing, coughing, talking. The portal of entry of virus is respiratory tract. Incubation period: 18 to 72 hours Complications : Pneumonia ,Guillain Barre syndrome ,Reye Syndrome ,Fatty liver. Lab diagnosis: virus isolation from nasopharyngeal secretions Govt. of India. influenza virus centre, Pasteur institute Coonoor, South India, Haffkine institute, Mumbai,School of tropical Medicine (Kolkotha),AIIMS (New Delhi,Vallabhai Patel Chest institute (Delhi), Armed Forces Medical College (Poone)
  • 26. Prevention : Take precautions • Good ventilation of public buildings. • Avoidance of crowded places during epidemics. • Encouraging suffers to cover their faces. • 7 stays at home at the sign of influenza. • Hygienic practices during handling of poultry products including: • hand washing, prevention of cross contamination and thorough cooking to > 70 ' c of poultry products. • Influenza vaccines
  • 27. Diphtheria Acute infectious and communicable disease characterized by involvement of the respiratory system, the local production of membrane and general symptoms caused by absorption of toxin . Agent: Cornybacterium diphterium Gram positive, Non sporing, Non capsulated and non motile, slender rod shaped bacteria. nasal Case carrier throat Case : Range from sub clinical to frank clinical cases . Temporary Carrier : State may last for about a month . Permanent Carrier : State may persist for a year or so unless the patient is treated. Source of infection
  • 28. Infective Material Nasopharyngeal Secretions . Discharge from Skin Lesions . Contaminated fomites and possibly infected Dust. Period of Infectivity Cases - 14 to 28 days Carriers - Longer periods Mode of transmission Mainly by droplet infection . ► Infected cutaneous lesions . By objects (ex : Cups, Thermometers) contaminated by the nasopharyngeal secretions of the patient Portal Of Entry Respiratory Route – Most common. Non respiratory routes ~ Skin – cuts, wounds & Ulcers. ~ Umbilicus of new born. ~ Eye, genitalia and middle ear. Incubation Period ~ 2 – 6 Days.
  • 29. Pertussis Whooping cough (pertussis)is an acute infectious disease, usually of young children caused by the bacteria bordetella pertussis. The Chinese call it a “Hundred Day Cough”. Agent Bordetella pertussis,Small gram negative,Aerobic coccobacillus Source •B.pertussis infects only man •S.O.I is a case of pertussis Infective material •Nasopharyngeal and bronchial secretions – bacilli occurs more in number. Infective period •Catarrhal stage Host Factors: Age-Disease of infants and preschool children •Highest incidence – below 5 years •High mortality - Infant below 6 months
  • 30. Environmental factors: Through out the year More cases – winter and spring Risk greater in lower social classes Infection generally lasts 2 to 3 weeks with 3 stages Catarrhal Stage • mild cough • Running nose • low grade fever • lasts for about 10 days Paroxysmal stage cough gets worse. cough is dry and harsh.cough ends with whoop sound on inspiration.child may vomit with the coughing and appear to be strangling on the vomit.cough can be started by many factors, including feeding, crying, or playing. Convalescent stage Vomiting and the whooping cough cease first. The cough usually decreases around the sixth week, but may continue on occasion for the next one to 2 months.
  • 31. Control Cases and contacts i. Cases Early diagnosis,isolation and treatment of cases and disinfection of discharges. Antibiotics – erythromycin, ampicilin, septran or tetracycline useful in controlling secondary bacterial infection ii. Contacts Infants and young children kept away. Those known to have been in contact – prophylactic antibiotic – days. iii.DPT vaccine
  • 32. Tuberculosis The Mycobacterium tuberculosis belongs to the genus Mycobacterium. • aerobic, • non motile, • rod-shaped bacteria. • Two distinguishing characteristics : • acid alcohol-fastness (AAFB), so strongly resistant, • slow growth. • Pulmonary TB is the most frequent presentation, • -Extra-pulmonary TB (e.g. miliary, skeletal, meningeal, gastro-intestinal) also occur, • particularly in children • immigrants and impaired immunity
  • 33.
  • 34. Primary TB develops within 1 or 2 years after an initial infection and, particularly in children, is often associated with disseminated disease. Post-primary TB develops later in life, and can be caused either by reactivation of bacteria remaining from the initial infection or by failure to control a subsequent reinfection. Post-primary TB is predominantly a pulmonary disease, involving extensive damage to the lungs and efficient aerosol transmission of bacteria. The risk of disease is highly dependent on: •the immune status of the host •co infection with HIV.
  • 35. Due to a combination of : •economic decline, •the breakdown of health systems, •insufficient application of TB control measures, •the spread of HIV/AIDS and •the emergence of multidrug-resistant TB. TB is on the rise in many developing and transitional economies •Who are on most risk? •Malnourished, The high number of imprisoned persons, Overcrowded conditions, Inadequate ventilation, Elderly, and Poor,migrants,smokers,other comorbidities,Chronicalcoholics,HIV/AIDS,Silicosis,Increasing drug resistance. .
  • 36. Control and prevention TB control and prevention Main strategies include: BCG vaccination Case finding Effective chemotherapy Health education Chemoprophylaxis In order to reverse the increasing trend in TB, effective control and prevention is required in all countries
  • 37. INTESTINAL INFECTIONS  POLIOMYELITIS  VIRAL HEPATITIS  ADD  CHOLERA  TYPHOID  FOOD POISONING  AMOEBIASIS  ASCARIASIS  HOOKWORM INFECTION  DRACUNCULIASIS
  • 38. POLIOMYELITIS Acute viral infection caused by an RNA virus. Primarily an infection of the alimentary tract but the virus may spread to CNS also in very small percentage of cases resulting in varying degrees of paralysis and possibly death. AGENT -Polio virus which belongs to the family picornaviridae. Classified into three types-Type 1,2,3. Type 1-most common and causes most epidemics. Type2-usually causes endemic infection. Type3-causes epidemics.
  • 39. Reservoir of infection:Man is the only known source of infection.Most of the infections are sub clinical. Infectious Material- faeces and oropharyngeal secretions of infected person. - The half life of virus is 48 hrs in sewage and spread can occur during this period Host Factors: • Age- mostly infancy and childhood. • Sex-it has been noted in the ratio of 3males to one female. • Immunity-immunity following infection is fairly solid although reinfection can occur since infection with one type does not protect completely against the other two type. • Pregnancy Environmental Factors: • More likely during rainy season. • Contaminated water,food,flies. • Survives for a long time in a cold environment. • Over crowding and poor sanitation
  • 40. Period Of Communicability- cases are most infectious 7 to 10 days before and after onset of symptoms. In faeces,virus is excreted commonly for 2 to 3 weeks ,sometimes as long as 3 to 4 months. Mode Of Transmission Faeco-oral route-this is the main route of transmission in developing countries. The infection may spread directly through contaminated fingers where hygiene is poor or indirectly through contaminated water,milk,foods,flies and articles of daily use. Droplet infection-occurs in acute stage where virus is in throat. Incubation Period – It is usually 7 to 14 days (range 3 to 35 days)
  • 41. Viral hepatitis Defined as inflammation of the liver. Viruses identified until now have been named as a,b c, d,e&g Agent Picornaviridae family Resistance: the virus withstands heating to 60deg c for 1 hour. Virus is inactivated by formalin,uvrays and by boiling for 5mins.Or autoclaving. Reservoir of infection:-human cases the only reservoir of infection. Asymptomatic (anicteric)infections are especially common in children.No evidence of chronic carrier state. Period of infectivity:-2weeks before to 1week after the onset of jaundice. Infective material: faeces;blood,serum & other fluids-during brief stage of viremia. Virus excretion:hav excreted in faeces for about 2weeks before and 1week after onset of jaundice. Incubation period- 15-45 days
  • 42. Environmental factors: In India associated with heavy rainfall. Poor sanitation and overcrowding -water borne and food borne epidemics. Faeco-oral route: major route of transmission. direct(person-to-person)contact or indirectly by contaminated water,food or milk. Food borne outbreaks (raw or inadequately cooked shellfish cultivated in sewage polluted water) Poor sanitation and overcrowding. PARENTERAL Hepatitis A rarely(blood and blood products/contaminated needles). SEXUAL TRANSMISSION This may occur mainly in homosexual men.
  • 43. PRIMARY PREVENTION HEALTH PROMOTION The people must be educated about proper sanitation and good personal hygiene (eg.washing oh hands after defaecation,before preparing food,before eating etc) Purification of community water supplies by flocculation,filtration and adequate chlorination Boiling water before drinking SPECIFIC PROTECTION This is means of a vaccine Sometimes passively by immunoglobulins.
  • 44. ACUTE DIARRHEAL DISEASE Passing of liquid or watery stools atleast 3 times in a 24 hour period . Consistency rather than the number of stools Acute :Sudden onset which lasts for 3-7days . Chronic :Diarrhoea lasting 3 weeks or more.
  • 45. Agent factors:Age : common in children between 6 months -2years. Incidence highest in age group 6-11months when weaning occurs. Nutrition ::: diarrhoea common in malnourished. Socioeconomic factors:Poverty. Incorrect feeding practices. Prematurity. Immunodeficiency. Lack of personal and domestic hygeine. Environmental factors:seasonal pattern in most developing countries . Cholera in winter. Rotaviruses in winter Shigella in dry summer
  • 46. CHOLERA An acute diarrhoeal disease. Cause by vibrio cholerae. A gram negative organism 5-10% of acute diarrhoeal cases. Profuse painless watery diarrhoea. Followed by vomiting, rapid dehydration and suppression of urine. Leading to hypovolemic shock & death in less than 24 hrs. Cholera stool: colour less watery fluid with flecks of mucus. Called as rice water stools.
  • 47. Mode of transmission:Occurs from man to man. 3 routes : 1. Faecally contaminated Water. 2. Contaminated food & drinks. 3. Direct contact. Agent factors: Causative org : vibrio cholerae Two sero groups – o1& non o1 Two biotypes - classical & eltor. Each biotype – 3 sero types: Susceptible to heat drying & acids. Resistance:resist high alkalinity,30 min by boiling at 56 c. Survival in water:grossly contaminated water - ganges donot survive Clean water survive up to 30 days. Survival in water influenced by ph,temp,salinity Susceptible to common disinfectants - eltor more resistant.
  • 48. Reservoir:human Source of infection : cholera stools & vomit. No.Of vibrios per ml of stool 1.Cases - 107 -109 2.Carriers - 102 -105 Pts excrete 10 – 20 lits of fluid. Cholera is dose related. Infective dose – 1011 orgs. Infection : ingestion of more than infective dose. Case is infectious for 7-10 days. Convalescent carrier infectious – 2 - 3 wks. Chronic carrier – up to 10 yrs. Chronic carriers less in classical more often in eltor.
  • 49. TYPHOID Severe, contagious,& life threatining disease.It is caused by contaminated food, drinks & water by bacteria called S.Typhi, which may result in fever with severe complications. Agent:- major cause S.Typhi,S.Paratyhpi a & b S.Typhi:- gram -ve, motile, peritrichate flagella .It has three main antigens o ,h ,vi. It was readily killed by drying,pasteurisation & common disinfectants. Man is a only reservoir of infection {cases & carriers } Carriers :temporary –the patient who shed bacilli >3months. Chronic - >1year. Convalescent- 3weeks - 3months.
  • 50. Source of infection:Primary source:- faeces & urine of cases & carriers. Secondary source:-contaminated water ,food,finger & nails. No evidence of typhoid bacilli excreted in sputum & milk. Social and environmental factors:Peak of incidence:-july & september.This period coincides with rainy season & an increase fly population. Social factors:-pollution of drinking water supplies, open air defecation & urination, low standards of food & personal hygeine & health ignorance,vegetables grown in sewage forms contaminated with water. IP:10 – 14 days.But it may be as short as 3 days or as long as 3 weeks depending upon of the dose of bacilli ingested. Modes of transmission:-faeco-oral route.Ingestion of contaminated water, milk & food.
  • 51. FOOD POISONING Acute gastro - enteritis caused by ingestion of food or drink contaminated by Living bacteria Bacterial toxins Inorganic chemical substances Poisons– plants and animals It is a point source epidemic- H/o of consumption of same food. Same symptoms in group of people. Attack of same persons at same time. Caused by following bacteria
  • 52. Bacterial poisoning: Infective and toxic types Caused by following bacteria • Salmonella • Staphylococcus • Botulism (cl.Botulinum) • Cl.Perfringens • B.Cereus Investigation of food poisoning Secure people list of involved and their history. ! Foods eaten during previous two days ! Symptoms- time of onset, type ! Personal data Laboratory investigations. ! Isolation of causative organism- stool,vomit, remnant food ! Stool samples of kitchen employees
  • 54. AMEOBIASIS Agent:E.Histolytica Reservoir:Man is the only reservoir of infection. The intermediate source of infection is the faeces containing the cysts. Most individuals infected with E.histolytica remain symptom free and are healthy carriers of the parasite. The carrier can discharge up to 1.5 x 107 cysts daily. Period of communicability : As long as cysts are excreted; the period may be several years, if carriers are unrecognized and untreated. Mode of transmission:Faeco-oral route This may readily take place through intake of contaminated water or food. Vegetables especially those eaten raw, from fields irrigated with sewage polluted water can rapidly convey infection. Viable cysts are found on the hands and under finger nails. This may lead to direct hand to mouth transmission.
  • 55.
  • 56. ASCARIASIS Most common helminthic infestation. Ascariasis is found worldwide. More than 1.4 billion people are infected. Prevalence of infestation during 1997 was 250 million Severe ascaris infections cause approx. 60,000 deaths per year, mostly children Agent :Ascaris Lumbricoides Reservoir of infection : man Infective material: feces containing Fertilized eggs Ascaris eggs are more likely to survive, and develop more rapidly, in shady, moist, clay soil Single female lays about 2 lack eggs per day.
  • 57. Mode Of Infection: Faecal-oral Route– Ingestion Of Food And Water Contaminated With Eggs. Eating Uncooked Food Grown In Contaminated Soil. Fingers Contaminated With Soil. Incubation Period: About 2 Months.
  • 59.
  • 61. DENGUE SYNDROME Spread by a bite of infected mosquitoes. Flavivirus (Dengue 1,2,3,4). Dengue virus manifests as: Dengue Fever: Flu like illness Dengue Hemorrhagic Fever: Severe often fatal Resevoir of infection Man is the main reservoir of virus. Monkey is the jungle reservoir in Malaysia and Africa. Host: Human Sex: Both Age: All Age groups
  • 62. Mode of transmission: human to human by mosquito bite. Vector:AEDES AEGYPTI- A polynesiensis, A sentellaris, A pseudosentellaris, A albopictus are the vectors. Female mosquitoes bites human during the day. Incubation period: 3-10 days (commonly 5-6 days). An infected person can’t spread the infectious to others but can be a source of dengue virus for mosquitoes for 6 days. Environmental factors: Breed in discarded types flower pots, old oil drums, water storage containers. Aedes breed in artificial collections of water
  • 63. LYMPHATIC FILARIASIS Worldwide prevalent, arthropod borne, causing permanent, long term disability & disfigurement & associated with social & economic stigma. It causes-Isolation -Psychological stress -Family discord -Impair employment -Impair mobility & activities
  • 64. AGENTS • W.BANCROFTI • B.MALAYI • B.TIMORI • Definite host is MAN. • Intermediate host is MOSQUITO. • Adult worms live in LYMPHATIC SYSTEM remain coiled together. • Male 2.5-4cm. & Female 8-10cm. • Mf are seen in blood, lung (capillaries), kidney,(glomerular tufts).
  • 65. Adult female worm gives birth to as many as 50,000 Mf/day (VIVIPAROUS) Enter the blood via lymphatics During blood meal, enter into mosquito Within 15-30 min.exsheathing in stomach Penetrate stomach wall & enter thoracic muscles Develop into first,sec,third stages Third stage migrate to the proboscis of mosq(infective) Through bite they enter humans
  • 66. Reservoirs-HUMANS - is a person with circulating Mf in peripheral blood. Host Factors MAN is a natural host. All ages are susceptible. Sex :higher in men. Migration: causes extension of filariasis into areas previously non endemic. Immunity: resistance to infection after many years of exposure. Environmental Factors A) Climate: 1)Mosquito-longevity & breeding 2)determines the development of parasite in the vector B) Town planning: rapid urbanization in INDIA -inadequate sewage disposal C) Drainage: breed profusely in polluted water. Common breeding habits 1)culex-cess pools, soakage pits, ill maintained drains, septic tanks, open ditches, burrow pits,etc. 2)mansonia-confined to areas where pistia plants are there.
  • 67.
  • 68. MALARIA 1.1 -- 2.7 million people are killed by this disease worldwide, each year.
  • 69. Host factors Age: Mostly all ages. Sex: Males at greater risk Race: Sickle cell trait -- Milder illness with P. falciparum Duffy –ve RBC -- Resistant to P. vivax Pregnancy: Primigravidae,IUD, premature labor or abortion Socio-economic development: Low Housing: ill ventilated & ill lighted ( indoor resting places) site, type of construction influence selection of control measures
  • 70. Population mobility: Internal migration Imported malaria [ Europe, N.America & temperate parts of the world ] Occupation: Mostly agrarian [rural backdrop] Human habits: Sleeping outdoors Nomads Refusal to accept spraying of houses Not using methods of personal protection like bed nets etc. Immunity: Collective immunity comes into play Immune mothers -- infants protected 3-5 months by maternal IgG Semi immune -- partially protected Active immunity is species specific Humoral and cellular responses help in protection
  • 71. Mode of transmission Vector transmission : Female Anopheline mosquitoes Direct transmission : Accidentally by hypodermic i.m & i.v injections of blood or plasma Congenital transmission : Rare Incubation period Usually not less than 10 days Varies with species P. falciparum malaria – 12 days [9-14 ] P. vivax – 14 days [8-17] Quartan malaria – 28 days [ 18-40] P. ovale – 17 days [16-18]
  • 72. Clinical features Fever with characteristic paroxysms Typical attack comprises of three distinct stages: Cold stage Severe headache, chilly sensation, vomiting Parasites demonstrable in blood Lasts for ¼ --1 hr Hot stage Burning sensation Hot skin and dry to touch Rapid respiration Lasts for 2 –6 hrs. Sweating stage Profuse sweating with fall in temp. Lasts for 2– 4 hrs Followed by an afebrile period – patient feels greatly relieved