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Lecturer 1

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Medical microbiology
It is concerned with
Aetiology
Epidemiology
Pathogenesis,
Diagnosis
Prevention
Control of microbial infection

Host-parasite relationship is mutualistic


If the parasites multiplies it is called infection
When it damages the tissue it is called disease

We have two types of pathogen


Opportunistic pathogen
Primary pathogen

Relationship btwn host and parasites


depends on
The population
The virulence(invasiveness, infectivity,
pathogenic potential, toxigenicity)
Host defense

Types of infections

Abscess
Acute infection
Bacteremia
Septicemia
Chronic infection
Overt infection
Focal infection
Latent infection
Localized infection
Mixed infection
Nosocomial infection
Pyogenic infection
Systemic infection
Toxemia
zoonosis

Pathogenesis of bacterial
disease

There must be reservoir host


The organism must be transmittable
Attachment and colonization
Invasion
Growth and multiplication within the
host
Leaving the host

Microbial products
Coagulase S.aureus
Colagenase Cl.spp
DNAsestaph,groupA
streptococcus,Cl.pefringes
Haemolysinsstaph, E.coli, enterococcus, strept
Hyaluronidase staph, Cl
Hydrogen peroxide staph
Streptokinase group A streptococcus
Leucocidin staph, pneumococci, streptococci

Determining the aetiology (causative


agent) of a disease is done by kochs
postulate
-Must be found in the host
-grown In pure culture
-inoculated into healthy animal
-must be recoverable

Normal microbial flora


Skin

Staphylococcus aureus and


staphylococcus epidermis

Respiratory tract

Staph aureus,
Branhamella catarrhalis
Haemophilus influenza

Mouth

Actinomycese, Lactobacilli,
Neiserria, Staphylococcus,
Heamophillus and streptococcus

Stomach

Helicobacter pylori

Intestine

E.coli, Klebsiella, proteus, candida


While the obligate anaerobes;Bacteriods, Clostridium,
streptococcus e.t.c
Staph, Enterococci, Bacteriod and
candida

Genitourinary tract

Staphylococcus
Commensals of the skin, nose, mucus membrane and
respiratory tract
Contracted from asymptomatc patient
Boils, Carbuncles, Folliculitis, scaled skin
Produce disease due to extracellular enzymes such as
B lactamase penicillin
Catalase- phaogocytosis
Haemolysin, liposis, nucleases, proteases

Staph au

Coagul
positive
Produc
yellow
on app
media
Manito

Causes abscess, hair follicle and tissue necrosis


Clinical symptoms of food poisoning- vomitting, abdominal
pain , cramps, vomitting and diarrhea. Incubation period is
about 1-8 hours
Diagnosis- sample is collected using swab, microscopy, gram
positive

streptococcus
S.pneumoniae, S.pyrogenes and
S.galactiae
Most infections of man are caused by
members of groupA Streptococcus
(S.pyrogen)

Streptococus pyogens
Sore throat(pharyngitis)
Fever, Sore-throat, Swollen cervical lymph nodes and exudates from the
Throats (FSST)
Scarlet fever
Streptococcal pyrogenic toxin (SPE)Erythrogenic toxins- Blood-Spleen-Reddish
rash on skin(EBSR)
Streptococcal toxic shock like syndrome
Higher fever, erythema and often a skin rash that may become gangrenous- necroticRenal failure and pneumonia are complications(FESGNR)

Puerperal fever (child birth fever)


Infection in Uterus after child birth
Inflammation of the uterus ffg by blood flow

Skin infections
May lead to lesions if there is prior injury of insect bite

Diagnosis
Throat swab, skin swab, B.agar alpha and beta haemolysis
Diff staph from strep by oxidase and catalsase (both neg for strept.)

Streptococcus pneumoniae

Gram positive in pairs.


Virulent factor capsule retard the rate of phagocytosis and also antigenic
The source of infection is usually exogenous
Predisposing factors for the disease to occur includes
Viral injury of respiratory tract, diabetes, inhalation of irritating substances and prolonged
hospitalization

Old are most susceptible


10-40% of human population are carriers
Focal infection leads to acute inflammatory reaction and infiltration of body fluids
Together with polymorphonuclear cells and RBC rapidly fill the lung lobe (for
lobar pneumonia)
In less severe PNS and macrophages take over
In serious case= pleurisy occurs which may lead to death
Symptoms:- rapid onset, shaking chills, fever, chest pain, cough xterised by
purulent sputum and rust colored
Diagnosis exudate examination, chest x-ray, sputum, blood and cerebrospinal
fluid collection and examination using direct microscopy

Enteric infection
This includes

Salmonella
Shigella
Yersinia
E.coli

Shigellosis (Bacilliary
infection)

Shigella dysentriae, Shigella flexneria, Shigella sonnei and


Shigella boydia
It is transmitted through faecal oral route
Fingers, Food, faeces, Flies

They produce endotoxin and exotoxin (SHIGA toxin) that do


not go beyond the colon
Pathogenesis
Contaminated Food ingestion
Penetrates large intestine through the stimulation of
endothelial cells
Invade neighboring cells
Inflammation of the submucosa together with sluffing of
epithelial cell
Ulcerative lesion occurs

Symptoms
Abdominal pains/cramps, diarrhea, fever, watery stool
(blood and mucus)
Dehydration and electrolyte imbalance may lead to death

Diagnosis
Isolation of the organism from faeces

Travellers diarrhea
It is a rapidly acting dehydrating condition, nuisance to
international travellers, it is xterised by profuse watery
diarrhea
ETEC enterotoxigenic e.coli
Produces heat stale and heat labile enterotoxix

EIEC enteroinvasive e.coli


Penetrates and multiply in the intestinal epithelial cells

EPEC enteropathogenic e.coli


Attach and brush boarder of intestinal epithelial cells to cause invasive
lesions

EHEC enterohaemorrhagic
Causes hemorrhagic colitis, produces shiga toxin

EAggEC enteroagglutinative e.coli


Attach to epithelial cells in localized areas

DAEC diffuslyadhering e.coli


Adheres to entire surface of epithelial cells

Diagnosis:- isolation using MA, EMB, etc.

salmonella
S.typhii, S.enteritidis, S.typhimerium,
S.paratyphii, S.choleraensis
S.typhimerium causes

salmonellosis/gastroenteritis
Reservoir (I.T of birds and animals)
Egestion of contaminated food
Incubation period of 8-48hrs
Invades and multiplies in submucosa
Produces enterotoxin that destroys the epithelial
cells
Symptoms
Abdominal pain, diarrhea, nausea and vomitting

S.typhii
causes typhoid fever/enteric infection
Consumption of contaminated food and water
Penetrates the epithelial lining of the small
intestine
Survives phagocytosis
1st week is xterised by fever, cramps and malaise
2nd week it infects the gall bladded
It sheds back into the intestine

Symptoms
Ulcerative lesion, abdominal tenderness, diarrhea,
vomitting exhaustion and death

Diagnosis
Widal test
Faeces blood and urine are the specimen used

Cholera

Vibrio cholerae; gram ve curved rod, natural habitat is


marine and shell fish
The organism is divided into two subgroups

The organism is also divided into two biotypes

01
0139

Classic
El Tor

The El tor biotype has been predicted as the major case of


epidemics of cholera

Incubation period of 1-2days


They adhere to intestinal mucosa but do not invade
Secrets choleragen labelled A and B
The A part enters the epithelial cells to activate the enzymes adenylate and
cyclase
These enzymes intiates hypersecretion of water and electrolytes with
abdominal cramps, vomitting, fever and watery diarrhea
Upto 10-15litres of water

Diagnosis
Culturing stool sample using blood agar and thiosulphate citrate bile
salt, the organism grows with a yellow color