1. Medical Microbiology Dr. Oruba lec.10

2. Host-parasite relationship

3. Host - Parasite Relationship
Human host is in contact with many microorganisms (normal flora) only a small number of these (primary and opportunistic pathogens) can cause disease.
Host-parasite relationships:
Is characterized by fighting of the organism to invade the body and the body defending itself by protective measures.

5. Pathogenicity
Pathogen
Disease

6. The pathogenic of bacterial infection includes initiation of the infectious disease and the mechanisms that lead to the development of signs and symptoms of disease
Characteristics of bacteria that are pathogens include transmissibility, adherence to the host cells, invasion of host cells and tissue, toxigenicity, and ability to evade the host's immune system. Many infections caused by bacteria that are asymptomatic.

7. Adherence ( cohesion, attachment) :-
The process by which bacteria stick to the surface of host cells. Once bacteria have entered the body adherence is a major initial step in the infection process.

8. Carrier : A person or animal with a symptomatic infection that can be transmitted to another susceptible.
Infection: multiplication of an infectious agent with in the body .multiplication of the bacteria that are part of the normal flora of the GIT, skin is generally considered as infection.
Invasion :the process whereby bacteria animal parasites, fungi, and viruses enter host cells or tissue and spread in the body.

9. Non pathogen: A micro-organism that does not cause disease; may be part of the normal flora.
Opportunistic pathogen: an agent capable of causing disease only when the resistance is impaired lie when the patient is immuno-compromised

10. Toxigenicity : the ability of a micro-organism to produce a toxin that contributes to the development of disease.
Virulence: the quantitative ability of an agent to cause disease
Virulence involves adherence, invasion and toxigenicity.-
Virulence is measured by the number of organisms required to cause disease.

11. Identifying bacteria that cause disease :
To improve establish that certain micro-organism can certain disease, several steps should be done (Koch's Potulates) these includes
Guidelines for establishing the cause of infectious disease

12. (Koch's Potulates):
disease in question and its distribution in the body should be in accordance with the lesion observed.
The micro-organism should be grown in pure culture in vitro (or outside the body of all the host) for several generations
When such a pure culture is inoculated into susceptible animal species, the typical disease must result.
The micro-organism must again be isolated from the lesion of such experimentally produced disease.

13. Virulence factors:
1-adherence factors a-surface charge b-receptors c-pili d-mucous layers 2- Invasion host cells epithelium, ingestion air-born droplets. 3-Toxins produced by bacteria are generally classified in two groups. a- Exotoxins :extracellular toxins b-Endotoxins (lipopolysaccharides of gram –ve bacteria)

14. Enterotoxin: Exotoxins associated with diarrheal diseases and food poisoning.
(eg, Vibro cholerae and Staphylococcus aureus produce enterotoxin)
all enterotoxins are exotoxins

15. Charateceristic of exotoxin and endotoxin (lipopolysaccharides)
Exotoxins
Endotoxins
Excreted by living cell in liquid medium
integral. Released on bacterial death.
produced by both gram-positive and negative bacteria
found only in gram-negative bacteria.
polypeptides
lipopolysacchanride complexes lipid A portion probably responsible for toxicity
unstable ,destroyed rapidly by heating at temperature 60c
stable ,withstand heating above 60c
highly toxic fatal to animals in micro-gram quantities or less
moderately toxic, fatal for animals in tens to hundreds of micrograms

16. converted to toxoids used to immunize eg, tetanus toxoid
non converted to toxoids
bind to specific receptors on the cells
do not bind to receptors on the cells
do not produce fever in the cells
produce fever in the host cell
frequently controlled by extra-chromosomal genes (eg plasmids)
synthesis directed by chromosomal genes.

17. 4- enzymes: several enzymes by invasive bacteria play a role in pathogenesis.
A-Tissue- degrading enzymes.
B-IgAl proteases.

18.  Tissue-Degrading Enzymes:-
Lecithinas (alpha toxin) produced by Clostridium Perfringens.
Lecithinase that hydrolyzes lecithin in the cell membrane
2.collagenase ,which degrades collagen the major protein of fibrous connective tissue ,and promotes spread of infection in tissue eg: c. perfringenes.
3.Coagulase ,which works in conjunction with blood factors to coagulase plasma.
4.Hyaluronidases , are enzymes that hydrolyze hyalaronic acid, a constituent of the ground substance of connective tissue .they are produced by many bacteria (eg).
5.streptokinase (fibrinolysin), a substances that activates a proteolytic enzymes if plasma .this enzyme is then able to dissolve coagulated plasma.
Many hemolytic streptococci produce the streptokinase.

19. 6.hemolysins, many bacteria produce substance that are cytolysine (hemolysins) in dissolve red blood cells RBC
7-Leukocidins---kill leukocytes(WBC)
B. IgAl proteases----allowing bacteria degrades secretory IgAl (pathogens) to attach to mucous membranes.

20.  Normal microbial flora of the human body.
-The term "normal microbial flora or microbiota" denotes the population of micro-organisms that inhabit the skin and mucous membranes of healthy normal persons.
The skin and mucous membranes always harbor a variety of microorganisms that can be in two groups:
-The resident flora
transient flora-
Resident: non pathogenic ,such organisms behave as opportunists and may become pathogens.
Transient :consists of non pathogenic or potentially pathogenic.

21. For example, streptococci of the viridians group are the most common resident organisms of the upper respiratory tract. If large numbers of them are introduced into the bloodstream ceg, following tooth extraction or oral surgery they may settle on deformed or prosthetic heart valves and produce infective endocarditis
Skin: staphylococcus epidermidis ,staphylococcus aureus corynebacterium species (diphtheroids) candida species
Pseudomonas aeruginosa
Propionibacterium SPP.
Nose: corynebacterium, staphylococci (S. epidermidis ,S. aureus) and streptococci.
Mouth: Viridans streptococci ,Neisseria ,Moraxella catarrhails ,diphtheroide ,Lactobacilli ,Fusibacterium ,Actinomyces.

22. Dental caries: Streptococcus mutans ,peptostreptococci ,actinomycetes.
GIT: Enterobacteriaceae except salmonella, shigella ,yersinia ,vibrio and campylobacters SPP.
RT: nonhemolytic and a-hemolytic streptococci and Neisseria ,staphylococci ,diphtheriods ,Haemophilus ,Pneumococci ,mycoplasma ,and prevotellae.
Genitalia: corynebacterium species ,lactobacilli species and nonhemolytic streptococci, non pathogenic neisseria species,
E-coli ,G-ve rods , ,
Candida albicans ,
A naerobes (clostridium and peptostreptococci species).
Conjunctiva: S.epidermidis ,
Non hemolytic streptococci ,
Neisseria and gram-negative bacilli
Haemophilus (moraxella species).

23. .

24. Typical stages of an infections:
The result of invasion or bacteria entrance to the body especially if more than one organ ,cause disease of the following clinical stages:
1-incubation period: which is the time between infection and the appearance of symptoms.
2-prodrome period is the time during which non specific symptoms occur such as fever ,malaise and loss of appetite occur.
3-the specific illness: is the time during which the characteristic features of disease occur.
4-the recovery period or convalescent period during which the patient return to healthy state.

25. Host defense:
1-Immunological system (Abs,etc)
2-Non specific mechanical & physical barriers.
- skin,multilayer & due to presence of germicidal sectors will hydrolyse.
-stomach ,acidity will decrease infective doses to half ,especially in alkaline bacteria.
-Lysozyme in salvia & tears .
-Cilia of mucous membranes of respiratory tract.
-Hairs of the nares (nose).
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-Normal flora of mucous membrane.
-Blood & lymph.
-Phagocytosis.
Certain types of Abs in the body (opsonins) can bacterial cell wall by opsonization to facilitate engulfment by phagocytosis

26. References:
1- Jawetz, Melnick, & Adelberg’s.( 2013). Medical Microbiology (Twenty-Sixth Edition).
2- Kenneth Todar. (2008).Todar’s Online Textbook of Bacteriology ,University of Wisconsin.

27. Thanks for your attention