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Other G-VE bacteria Course: Medical Bacteriology Lec. No 7 4 th Grade Fall Semester 2021-2022 Dr. Salah Tofik Balaky Ph.D. Medical Microbiology [email protected] 12/12/2021

Other G-VE bacteria Course: Medical Bacteriology Lec. No 7

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Page 1: Other G-VE bacteria Course: Medical Bacteriology Lec. No 7

Other G-VE bacteria

Course: Medical Bacteriology Lec. No 7

4th Grade – Fall Semester 2021-2022

Dr. Salah Tofik Balaky

Ph.D. Medical Microbiology

[email protected]

12/12/2021

Page 2: Other G-VE bacteria Course: Medical Bacteriology Lec. No 7

The Shigellae

The natural habitat of shigellae is limited to the intestinal

tracts of humans and other primates, where they produce

bacillary dysentery. Shigellae are slender G-ve rods

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Page 3: Other G-VE bacteria Course: Medical Bacteriology Lec. No 7

Antigenic Structure

Shigellae have a complex antigenic pattern. There is great

overlapping in the serologic behaviour of different species,

and most of them share O antigens with other enteric bacilli.

The somatic O antigens of shigellae are lipopolysaccharides.

Their serologic specificity depends on the polysaccharide.

There are more than 40 serotypes.

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The classification of shigellae relies on biochemical

and antigenic characteristics.

Species Group and

Type

Mannitol Ornithine

Decarboxylase

S. dysenteriae A -VE -VE

S. flexneri B +VE -VE

S. boydii C +VE -VE

S. Sonnei D +VE +VE

Page 5: Other G-VE bacteria Course: Medical Bacteriology Lec. No 7

Shigellae Pathogenesis: Shigella infections are almost

always limited to the gastrointestinal tract. The infective dose

is on the order of 10³ organisms (whereas it usually is 10⁵–

10⁸ for salmonellae and vibrios). The essential pathologic

process is invasion of the mucosal epithelial cells by induced

phagocytosis, escape from the phagocytic vacuole,

multiplication and spread within the epithelial cell cytoplasm,

and passage to adjacent cells.

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Page 6: Other G-VE bacteria Course: Medical Bacteriology Lec. No 7

Shigellae Toxins

1. Endotoxins: Upon autolysis, all shigellae release their

toxic lipopolysaccharide. This endotoxin probably contributes

to the irritation of the bowel wall.

2. Shigella dysenteriae exotoxin: Acting as a neurotoxin,

this material may be contribute to the extreme severity and

fatal nature of S. dysenteriae infection and to the central

nervous system.

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Salmonellae are vary in length and most isolates

are motile with peritrichous flagella. They are small

Gram-negative bacillus. The genus Salmonella

contains over 2,000 sero-species and is one of the

most important pathogens in the family

Enterobacteriaceae. The most important

Salmonella species is S. enterica.

The Salmonellae

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Bacterial antigens

Usually motile (H antigen)

Possess polysaccharide capsule (K antigen on most

Salmonella spp. or Vi antigen of Salmonella typhi and

Salmonella paratyphi)

Specific O antigens

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Pathogenesis

Salmonellae are often pathogenic for humans or

animals. They are transmitted from animals and

animal products to humans.

1. Enteric fever (Typhoid and less severe

Paratyphoid fever)

2. Non-typhoid salmonellosis

3. Bacteremia

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Entric fever

(Typhoid and paratyphoid fever)

Typhoid is caused by Salmonella enterica subsp.

enterica serotype Typhi (Salmonella typhi) and

paratyphoid is caused by Salmonella enterica

serotypes S. paratyphi (A, B and C). Consumption

of contaminated food and water or contact with a

patient or carrier of the disease are common

vehicles of infection.

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Salmonella generally cause illness by localised

infection of the gastrointestinal tract. Infection is

characterised by colonisation and attachment of

the bacteria to epithelial cells, and subsequent

invasion of the intestinal tissue. During this

invasive process, a heat-labile enterotoxin is

secreted by the bacterium that precipitates a net

efflux of water and electrolytes into the intestinal

lumen resulting in diarrhoea.

Typhoid and paratyphoid fever

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Fever, enterocolitis with diarrhoea and abdominal

pain, hepatosplenomegaly, bradycardia and rose

spot on trunk

Symptoms:

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Non-Typhoid SalmonellosisThe disease caused by over 2,000 Salmonella

serovars. The most frequently reported one from

humans is S. serovar typhimurium and S. enteritidis.

The initial source of the bacterium is the intestinal

tracts of birds and other animals. Humans acquire the

bacteria from contaminated foods such as beef

products, poultry, eggs, egg products, or water. Once

the bacteria are in the body, the incubation time is

only about 8 to 48 hours.

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Non-Typhoid Salmonellosis …The disease results from a true food- borne infection

because the bacteria multiply and invade the

intestinal mucosa where they produce an enterotoxin

and cytotoxin that destroy the epithelial cells.

Abdominal pain, cramps, diarrhoea, nausea, vomiting,

and fever are the most prominent symptoms, which

usually persist for 2 to 5 days but can last for several

weeks.

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This is associated commonly with S. choleraesuis.

Following oral infection, there is early invasion of

the bloodstream (with possible focal lesions in

lungs, bones, meninges, etc), but intestinal

manifestations are often absent.

Bacteremia

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In the early 1900s there were thousands of typhoid

fever cases, and many died of the disease. Most of

these cases arose when people drank water

contaminated with sewage or ate food prepared by

individuals who were shedding the typhoid fever

bacterium (Salmonella typhi). The most famous carrier

of the typhoid bacterium was Mary Mallon.

“Typhoid Mary”

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Between 1896 and 1906 Mary Mallon worked as a cook

in seven homes in New York City. Twenty-eight cases

of typhoid fever occurred in these homes while she

worked in them. As a result the New York City Health

Department had Mary arrested and admitted to an

isolation hospital on North Brother Island in New York’s

East River.

“Typhoid Mary”

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Examination of Mary’s stools showed that she was

shedding large numbers of typhoid bacteria though she

exhibited no external symptoms of the disease. An

article published in 1908 in the Journal of the American

Medical Association referred to her as “Typhoid Mary,”

an epithet by which she is still known today. After being

released when she pledged not to cook for others or

serve food to them.

“Typhoid Mary”

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Mary changed her name and began to work as a cook

again. For five years she managed to avoid capture

while continuing to spread typhoid fever. Eventually the

authorities tracked her down. She was held in custody

for 23 years until she died in 1938. As a lifetime carrier,

Mary Mallon was positively linked with 10 outbreaks of

typhoid fever, 53 cases, and 3 deaths.

“Typhoid Mary”

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The pseudomonads are gram-negative, motile,

aerobic rods some of which produce water-soluble

pigments. Pseudomonads occur widely in soil, water,

plants, and animals. Pseudomonas aeruginosa is

frequently present in small numbers in the normal

intestinal flora and on the skin of humans and is the

major pathogen of the group.

The Pseudomonad Group

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P. aeruginosa is widely distributed in nature and is

commonly present in moist environments in hospitals.

It causes disease in humans with abnormal host

defences.

Pseudomonas aeruginosa

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P aeruginosa is motile and rod-shaped, G-ve and

occurs as single bacteria, in pairs, and

occasionally in short chains. P. aeruginosa is an

obligate aerobe that grows readily on many types

of culture media, sometimes producing a sweet

or grape-like odour. Some strains hemolyzes

blood.

P. aeruginosa

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P. aeruginosa forms smooth round colonies with

a fluorescent greenish colour. It often produces

the non-fluorescent bluish pigment pyocyanin,

which diffuses into the agar.

P. aeruginosa

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Pili (fimbriae) extend from the cell surface and

promote attachment to host epithelial cells.

The exopolysaccharide is responsible for the

mucoid colonies seen in bacterial cultures

The lipopolysaccharide, is responsible for many of

the endotoxic properties of the organism.

Antigenic Structure & Toxins

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Many strains of P. aeruginosa produce exotoxin A,

which causes tissue necrosis and is lethal for

animals when injected in purified form. Antitoxins

to exotoxin A are found in some human sera,

including those of patients who have recovered

from serious P. aeruginosa infections.

Antigenic Structure & Toxins

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P aeruginosa is pathogenic only when introduced

into areas devoid of normal defenses, eg, when

mucous membranes and skin are disrupted by

direct tissue damage. The bacterium attaches to

and colonizes the mucous membranes or skin,

invades locally, and produces systemic disease.

These processes are promoted by the pili,

enzymes, and toxins

P. aeruginosa pathogenesis

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Next lecture

H. pylori and Campylobacter

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Any questions or Comments?