Infectious Diseases
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Transcript Infectious Diseases
Infectious Diseases
By
Andoh Wilson
Infectious Disease Terms
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Epidemiology
Epidemic
Endemic
Pandemic
Pathogen
Opportunist
Nosocomial
virulence
Normal Micro flora & its importance
1. Prevent the growth of pathogens
2. Stimulate the immune system to produce
antibodies that cross-react with invading
pathogens
3. Aid in digestion of cellulose in ruminants.
4. Produce essential nutrients
Koch’s Postulates
1. The same pathogen must be present in
every case of the disease;
2. The pathogen must be isolated from the
diseased host and grown in pure culture;
3. The pathogen from the pure culture must
cause the disease when it is introduced into
a healthy but susceptible organism.
4. The pathogen must be isolated from the
inoculated animal and be shown to be the
original organism.
Modifications to Koch’s Postulates
1. Some infectious agents cannot be
cultured e.g. prions
2. Some pathogens have non-virulent
strains whose presence does not link
them to a disease. E.g. non
encapsulated Diplococcus pneumoniae
Types of Pathogens
1. Bacteria
1. Gram positive
2. Gram negative
3. Acid-Fast e.g. Mycobacteria
1. Spherical described as cocci
2. Rod shaped described as bacilli
Gram Positives
•
Unique Features
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–
–
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Thick peptidoglycan wall
No periplasmic space
No outer membrane (capsule)
E.g. Streptococcus pyogenes,
Staphylococcus aureus, Bacillus anthracis,
Clostridium tetani
Gram Positive wall
Gram Negatives
• Unique features
– Thin peptidoglycan wall
– Has periplasmic space containing different
degradative enzymes such as
deoxyribonucleases, -lactamases and
proteases
– Outer membrane containing lipid A, an
endotoxin
– E.g. Neisseria, Salmonella typhi, E. coli,
Yersinia pestis, Vibrio cholerae
Gram Negative wall
Types of pathogens
2. Parasites (Eukaryotic Pathogen)
1. Fungi e.g. Candida, Aspergillus
2. Protozoa e.g. Plasmodium, Schistosoma
3. Worms e.g. Ascaris, Taenia
Types of pathogens
3. Viruses
1. Are pieces of DNA or RNA surrounded by
protein coat. The may be
2. Encapsulated e.g. HIV, HBV, measles,
mumps, influenza, rabies
3. Non-encapsulated e.g.adenoviruses, HPV,
Polio
Viruses
Modes of transmission
1. Direct contact e.g. touching,
handshaking, or sexual intercourse
2. Indirect contact e.g. food, water or
droplets in air;
3. Animal vectors e.g. insect bites in
malaria, plague and oncho, dog bite in
rabies
Pathogenesis
• Sequence of activities
1. Transmission of causative agent to
susceptible host;
2. Adherence of the agent to a target tissue;
3. Colonization and invasion;
4. Damage to host by toxins or other
mechanisms;
5. Exit from host;
6. Survival outside host long enough for step
1 to occur.
Virulent Factors
•
•
For all pathogens there is an infective
dose and a lethal dose.
Virulent factors that confer pathogenicity
include;
1.
2.
3.
4.
5.
6.
Pili that facilitate attachment;
Capsules that interfere with phagocytosis
Exotoxins
Endotoxins
Proteases that break down antibodies
Ability to vary antigens to evade antibodies
Bacterial Pathogenesis
1. Toxin production. Toxins fall into two
categories; exotoxins and endotoxins.
2. Invasiveness, where bacteria grow to
large numbers locally and produce
enzymes that damage host tissues.
exotoxins
1. Heat labile (60-100 degrees for 30 mins)
proteins produced and released by both
gram positive and gram negative
bacteria.
2. Produced by bacteria such as
Clostridium (neurotoxins) and Bacillus
(enterotoxin) (+) and E. coli and Vibrio
(enterotoxin) (-)
endotoxins
1. Are heat stable (100 degrees for 1 hr)
lipopolysaccharide produced only by
gram –ve bacteria. They remain attached
to cell wall.
2. Cause fever and shock and is of lower
toxicity compared to exotoxins.
3. Produced by bacteria such as
Salmonella
cholera
1. Causative Agent: Vibrio cholerae
2. Symptoms: severe diarrhoea up to 20
liters a day of “rice water stool”, vomiting,
muscle cramps caused by loss fluid and
electrolytes.
3. Pathogenesis: Vibrio adheres to the
small intestinal lining, multiply and
produce the enterotoxin choleragen
which causes the accumulation of cAMP.
An increased secretion of water and
electrolyte from the cells results
Cholera
4. Epidemiology: Feacally contaminated
water, crabs and vegetables fertilized
with human faeces. Has been eradicated
most developed countries but a new
strain discovered in 1992 is threatening
another pandemic.
Cholera
5. Incubation period: 12-48 hours
6. Lab diagnosis: Microscopy, culture of
sample from faeces or vomit.
7. Prevention: Purification of water, washing
of hands.
8. Treatment: administration of solution of
glucose and electrolyte orally or
intravenously; tetracycline antibiotic orally
malaria
1. Causative Agent: Plasmodium (4 species)
2. Symptoms (Clinical features): fever, chills,
anaemia, headache, nausea, shivering,
convulsions (esp. in under 5 yr olds)
enlarged spleen.
3. Pathogenesis: site of action of pathogen
include: liver, RBC, brain. The vector,
female Anopheles mosquito, transfer
pathogen during feeding.
malaria
4. Epidemiology: Endemic in 91 tropical and
subtropical countries. Invade the liver 1st
and move to reproduce in RBCs resulting
in their rupture and the associated chills.
5. Incubation Period: 1 – 2 weeks.
6. Lab diagnosis: Microscopy.
An Infected RBC
Malaria - Prevention
1. Reduce the number of mosquitoes;
destruction of larvae and adult
mosquitoes by biological and chemical
control methods
2. Avoid being bitten; protective clothing
and creams, treated bed nets
3. Use of drugs to prevent infection;
chemoprophylaxis
Malaria -Treatment
• Combination therapy: Artesunate
Amodiaquine
Tuberculosis
1. Pathogen: M. tuberculosis (pulmonary TB);
M. bovis(GI TB)
2. Transmission: airborne droplets (NB MTB is
dessication resistant and survives in dried
sputum); unpasteurized milk.
3. Clinical features: prolonged coughing
sometimes with bloody sputum, shortness of
breath, fever, sweating , weight loss
Tuberculosis
4. No toxin production. Pathogenicty is by
invasiveness that produce characteristic
lesions in the lungs.
5. Epidemiology: pathogen triggers acute
inflammatory response + forms tubercle –
giant cells containing MTB and surrounded
by epithelial cells. Tubercles heals by
fibrosis and calcification. Can desseminate
via bloodstream to other internal organs