types of bacteria
spherical (cocci)
rod (bacilli)
spiral (spirilla)
comma (vibrios)
corkscrew (spirochaetes)
cocci
gram +
staphylococcus
streptococcus
enterococcus
there are much more gram+ cocci, but the named ones are the most imortant for the human health
gram -
neisseriae
gonococcus
meningococcus (both diplococci)
staphylococci
differentiation due to their coagulase activity
=> coagulase: crucial enzyme to differenciate staphylococci
positive coagulase activity:
staphylococcus aureus
-> to use blood for energy production
-> to perform hemolysis
negative coagulase activity: staphylococcus epidermis
(name because of golden colour of the skin)
cogulase+
member of the normal microbiota in nose and skin
active in numerous diseases:
skin: abscess, folliculitis
nose: sinusitis
gut: food poisoning
bone/joint: osteomyelitis, septic arthritis
(not 100% clear how bacteries come to the bone; often after surgery)
bacteremia (sepsis) -> endocarditis!
(live in the blood and replicate in high numbers)
virulence factors:
enzymes: coagulase
toxins:
superantigens (toxic shock syndrome)
exfoitative toxins
membrane toxins (alpha, beta, delta)
type VII secretion system (one type of a very effective secretion for b. to defend/protect themselves)
small RNA
DNA repair (s.a. has the ability; antibiotics that affect (destroy+fragmentate) DNA are no longer effective
post-transcripitonal regulation
PROBLEM:
-> due to ubiquitous presence adapted to a lot of conditions
multiple resistancies (as it develops resistancy quite rapidly)
staphylococcus epidermis
coagulase-
s.e. always present on healthy skin (within the cornea layer of the skin; each manipulation of the skin, like entering a needle, can lead to the entering of the bacterium into a deeper layer)
skin microbiota (microbioma) memeber, and crucial for normal fct of the skin
influences odor (foot)
forms biofilms (resistance; protects the outer skin from the entering of fungi)
Acne vulgaris (+ cutibacterium acnes) (as often resistancies against antibiotics, cleaning of the skin is more important than medic treatment)
often antibiotic resistances
-> crucial memeber differenciating the content of the sweat glands
-> s.e. especially increased in conditions where is no free air around
streptococci
differentiation due to their hemolytic activity:
alpha hemolysis
streptococcus pneumoniae (vaccines due to its importance!!)
beta hemolysis (hemolytic activity)
streptococcus pyogenes
streptococcus agalactiae
gamma (no) hemolytic activity
enterococcus faecalis, faecium)
streptococcus pneumonia
a-hemolytic activity
does not belong to the microbioma on the skin
transduced via the air ways, can spread all over the mucous from the nose into the lungs
affects very often the lungs themselves (name)
-> dangerous, because oxygen exchange is disturbed by having liquid in the alveoli (empyema)
-> as they can reach the heart region through the lungs, also the heart can be affected by an empyema in the pericardium
-> from aleveoli can easily enter the blood system and lead to a scepticaemia
can also lead to arthritis or osteomyelitis
as spreading via the blood, can also affect the brain and form a meningitis
why is it so dangerous?
is a bacterium with a capsule, so it is better protected and the IS has more difficulties to act against the bacterium
produces enzymes which destroy alveolar tissue
has choline-binding proteins present in the cell wall, so can affect the nervous system
beta hemolytic activity
found more frequently than other bacteria on the skin and in the mucous
active in numerous diseases
streptococcal pharyngitis
skin: folliculitis, cellulitis, impetigo (Eiterflechte, Grind)
scarlet fever (Scharlach)
rheumatic fever
postinfectious glomerulonephritis
Penicillin!!! (still sensitive to penicillin as it does not cover up plasmids for resistance)
-> more important for avoiding the postinfectious diseases such as glomerolunephritis)
=> beta hemolytic activity of streptococci is always in combination with high virulence and dangerous conditions
first, intestinal colonization and destruction of the epithelium of the gut, from there via transcystosis into blood vessels, blood takes them to the brain
-> possible meningitis
streptococci / enterococci
gamma hemolytic activity
possibly caused diseases:
urinary tract infection
sepsis
meningitis
endocarditis
WHO: bio-indicator for water quality in pools + ocean
neisseriae: gonococcus
gram-
only sexually transmitted (infection depends on where sexual contact occured):
urethritis (proctitis / pharyngitis)
arthritis
dermatitis
prevention: latex barriers
treatment: single injection of ceftriaxone
newborn conjunctivitis (outer eye)
can become so severe until occurance of blindness
erythromycin gel prophylaxis (aggressive silver nitrate prophylaxis no longer used)
neisseriae: meningococcus
form a thick capsule in addition to the wall
-> immune system has difficulties to identify and act against them
-> only region is within the spleen (resectomy of
spleen is a problem!!!)
meningitis: lethality 10%!
-> normal adult immune system is stable enough to fight m. (bigger problem for children, small children and newborns)
-> healthy adults normally do not need vaccination
-> but for example, if spleen was resected
sepsis:
purpural rush (Henoch-Schönlein)
specific sign of condition seen on the skin -> small hematomas within the skin without mecanic causes
Waterhouse-Friedrichsen syndrome (adrenal gland insufficiency)
disseminated intravascular coagulation (DIC)
vaccination: very effective in forming antibodies
group of rods
(also divided in gram+ and gram-)
have some specific metabolic activity
gram+:
- Listeria monocytogenes, Corynebacterium diphtheriae
-> aerob, no spores
- Bacillus anthracis
-> aerob, spores
- Lactobacillus, Bifidobacteria, Actinomyces
-> (non) aerob, no spores
- Clostridium botulinum, C. perfringens, C. tetani, C.
difficile
-> anaerob, spores
gram-:
- Pseudomonas aeruginosa
Bordetella, Legionella, Haemophilus
-> aerob
listeria monocytogenes
most common type of rod bacteria
great impact on human because of high mortality
-> 70%!!!
virulence factors
-> does not live outside of cells, so not seen by IS (foreces the cells to take them up and can then live, act and replicate without being seen by IS)
-> does not have to leave cell to infect a next one, but builds extrusion/extension to contact next cell
=> UNIQUE FEATURE
-> IS strictly limited to signals outside of cells:
decreased production of MHC-I protein, which will lead to destruction of cell by IS
PROBLEMS:
can affect neural cells which cannot be destroyed by IS; and inflammatory process is not effective as bacteria are inside the cells -> inflammation of brain can get very severe; only a few antibiotics for treatment as they have to enter the blood-brain-barrier, and treatment with chemicals within cells always means an affection of the metabolic activity of the cell itself
can lead to a sepsis, when at a certain stage let out of cells into intracellular space; and when in the blood, again they can spread to the brain
-> mainly in animal products: raw milk and products made
out of it, therefore heating of milk and no use of raw milk
LIFE CYCLE
1) listeria enter the intestine
2) can penetrate through epithelium
3) then infects the lymphatic cells
4) and then reach the lymph nodes and enter the blood
-> thatwise able to reach organs - mainly liver and spleen -
unseen by IS
-> in spleen able to infect erythrocytes
-> spleen enlargement typical sign for listeria infection
-> most problematic tissue again is the brain tissue
BUT
-> pregnancy:
can enter the placental barrier and reach the fetus
within the fetal tissue it will destroy nervous system
-> growth no longer possible and will lead to abortion
(dead of fetus)
=> no consumption of raw food!!!
cornybacterium diphteriae
gram+
-> toxins lead to problems not bacterium itself, so only toxin producing bacteria of c.diphteriae is a problem for human condition
-> specific appearance, which allows differenciation from other rods by microscopy
-> as toxine has been major problem in the 19th century, vaccination already for over 100yrs!!! and diphteriae is no problem in the population
first with another corynebacterium, nowadays with toxine)
WHAT DOES TOXINE DO?
c.diphteriae enters airways and proliferates in the mucous
extracellular bacterium, therefore IS can react
at the moment, it produces toxins, a pseudo-membrane formation on the surface of the epithelium occurs, can extend to nasal region and airways + larynx (!) -> inflammation will start there which causes a swelling that can lead to severe problems with breathing and therefore also dead
in a second step, the toxine can enter the blood from the epithelium -> secondary diseases of central nervous system, kidneys and heart
-> necessity to react early, that these membranes will not spread and extend in more dangerous sites and to avoid toxemia (that the toxine does not reach the blood) (which the IS can do easily when having had contact with toxine before)
bacillus anthracis
spore forming, four sites where toxin can act
1) skin: boil-like lesions, like a large burning
2) injection: can reach the whole body via the blood, can perform these boil-like changes in the inside: most feared that changes reaches the lungs
3) lungs (via breathing): not immediate but delayed reaction, so long period with just coughing and not feeling well (not linked to b.a., yet); can then lead to severe pneumonia, and leaving the lung tissue also mediastinitis (inflammation of CT between the lungs) -> crucial and dangerous condition
4) GI tract (gut): symptoms such as diarrhea as main symptom
spores easily to be spread; used for bioterrorism; rapid reaction as spores contain some toxin and one does not have to wait until the spores witch back to metabolic stage
aerob bacterium, so easily reactivation of metabolic stage in sites with oxygen, which is everywhere with blood supply
WHAT DOES THE TOXIN MAKE?
produces edema
and too much fluid outside the cells in the extracellular part of the tissue -> interrupted nutrition
or fluid in lumen of gut -> severe loss of liquid (diarrhea)
=> capsule protects from phagocytosis
lactobacillus and bifidobacteria
typical appearance of two large bacteria lie next to each other and form one entity -> name BI- comes from this aspect
LACTO- -> mainly found in milk
has specific feature that it interacts with sugar which it reduces to lactic acid -> oral cavity
lactic acid can interact with extracellular material strcts in the teeth -> caries within the teeth
in other areas we want to have acid situations to prevent spreading of other bacteria -> GI tract and vagina, are therefore seen as probitiotic bacteria
are part of normal microbioma; able to proliferate when IS unstable
involved in GI tryptophan metabolism -> transform it into 3 other elements:
1) IPA -> protects the brain and its activity
2) I3A -> stimulates the immune cells in the intestine
3) indole -> helps the liver; protective against vascular diseases
clostridium bacteria group
group of gram+ rods
C. botulinum: botulinum toxin (neuromuscular blockage)
C. perfringens: food poisoning, fasciitis, gas gangrene
C. tetani: tetanus toxin (muscle spasms)
C. difficile: multiple toxins (diarrhea, colon cancer)
bacteria mainly need aerobic conditions
spore building
all bacteria are able to produce toxins, which mainly interact with nervous system -> life threatening conditions possible!!!
c.botulinum toxin and c.tetani toxin partly used as medication, with opposite mechanisms -> botulinum toxin (botox) relaxes muscles (neuromuscular blockage by blocking acetylcholine release and destroying adhesion element necessary for vesicles to attach to outer membrane), while tetani toxin leads to constant contraction as inhibiting transmitters are blocked (muscles can get damaged (until loss of muscle tissue) due to lack of relaxation which is crucial for nutrition and oxygen support)
c. perfringens taken up with food
toxin is able to destroy epithelial lining of the gut
-> inflammatory reaction with invasion of many immune cells
-> activity of epithelium no longer possible => no reuptake of any substances; digestion severly affected, which makes poisoning with c.perfringens very critical
pseudomonas perfringens
gram- rod
ubiquitous present, but under normal health conditions not problematic:
hospital-acquired infections -> pneumonia + sepsis
predominant risks: cystic fibrosis, immunocompromised
highly adapted to antibiotics
does not produce toxin, but interaction with tissue problematic
bordatella
produces toxin
affects mainly tissues with cynocilium-like appearance -> respiratory tract, the lungs, the trachea, the oral site
only seen in humans -> vaccination very effective strategy to get rid of b.
legionella group
first identified 1976
like to enter cell system and live within cellular condition (appropriate nutrition and energy support)
live in amoebae (protozoa) which live in humid environments and get destroyed as soon as there is ‘moving’ water -> showers (if not used, amoebae spread, and when used again, amoebae get destroyed and legionella are free, and one can get into contact, and by inhaling, they can enter respiratory tract
-> upper respiratory tract: pontiac fever
-> lungs: atypical pneumonia: legionnaires disease
with a strong IS, one will develop pontiac fever but no legionnaires disease (often in older people)
prevention: no aerosolic contact with long-time stagnant water
haemophilus influenzae
gram- rod (red color in staining)
form a capsule -> need specific immunological reaction (which is not so well developed in infants and children -> problem to defend these bacteria)
as the name indicates, during infection it has similar symptoms as other flu performing microorganisms:
-> sinusitis
-> otitis media
-> infection of the larynx, bronchi and lungs
higher aggressivity, likes to invade the tissue, then can extend and form a bacteriemia -> leads to distribution all over the body, most feared if reaches the brain -> meningitis
-> vaccination (most reasonable for children up to 5, then IS developed enough); only against type b (hib), so one can get infection with other hi type
enterobacteriaceae
vibrio
salmonella
shigella
escherichia
yersinia
helicobacter pylori
=> widely spread, not only as human pathogens, but in the whole environment (insects, water, vegetation, animals)
=> very important for the whole system, as they support the environment
=> can therefore not be erased and a strategy against them has to be individual on each human affected by them
=> erasing them would harm ourselves, e.g. with e.coli
vibrio cholerae
Bild vor vibrio cholerae
intracellular (difficult for IS to react against it), non-spore forming, facultative anaerob
fecal-oral transduction
flagellated
two species -> s.bongori + s.enterica
two forms of disease -> typhoidal + non-typhoidal
non-typhoidal salmonellosis spread worlwide
usually food-borne, through oral consumption of non-cooked or -heated eggs, chicken, meat, raw vegetables and fruit
can be spread person-person -> causes typhoid fever (Typhus)
incubation time: 12-24hrs, but can be up to 72hrs
symptoms: enteritis with diarrhea without any obvious cause, blood in the stool
typhoid fever: stomach pain, general system diseases, pneumonia, joint arthritis, kidney failure
usually spreading more due to contaminated excretions
long-term problems: irritable bowel syndrome,
inflammatory bowel disease
prevention: clean environment, washing hands, washing the fruit, boiling the water, etc
gram- rod bacterium
non-motile, facultative anaerob, non-spore forming
intracellular
4 subgroups
s.dysenteriae
s.flexneri
s.boydii
s.sonnei
-> dependend on subgroups, different symptoms form, and different way of acting in the body
pathophysiology
-> transmitted via contaminated food or water, poor sanitary conditions or person-to-person contact
-> only a small number (10-100) of shigellae needed to cause lifethreatening shigellose of high resistance to gastric acid
-> enters the epithelium, and because of rapid renweal of epithelial cells (within 48hrs), normally infection does not last long
-> has the ability to develop intracellular motility, which makes an infection last longer, as it remains hidden from the IS
-> production of toxins as another virulent factor
symptoms:
-> usually manifest after 24-48hrs
-> without treatment these can last 7-10 days
-> fever
-> watery diarrhea, in severe cases mucous-bloody dysentery (Durchfall/Ruhr)
-> dehydration
-> vomiting
-> abdominal pain and tenderness
-> arthritis
-> HUS: hemolytic urine syndrome
treatment:
-> rehydration
-> antibiotics
escherichia coli
Gram- rod, non-spore-forming, facultative anaerobic, motile (flagella)
part of our microbioma in the intestines
provide vitamin K for the body (can lead to need of oral supplementation of vit K, if e.coli is affected by antibiotics taken against other diseases
most widely studied bacteria
pathogenesis:
3 known antigens, which interact with IS
-> O-antigen: lipopolysaccharide on outer membrane
-> K-antigen: capsular polysaccharide (protective
element)
-> H-antigen: flagella (reacts with it; finding niches for
better survival)
depending on symptoms, different pathogenic subtypes:
-> more toxic activity: ENTEROTOXIGENIC e.coli (ETEC)
-> hemorrhage: ENTEROHERMORRAHRGIC e.coli (EHEC)
-> ENTEROAGGREGATIVE e.coli (EAEC)
-> ENTEROINVASIVE e.coli (EIEC)
patheogenicity:
-> Gastrointestinal diseases (Diarrhea)
-> Urinary tract infection (UPEC): bladder, kidneys, prostate
-> Neonatal meningitis (NMEC)
gram- coccobacilli
facultative anaerob
y. pestis -> bubonic or pneumonic plague
y.enterocolitica -> gastroenterocolitis (yersiniosis) in
humans
-> food-borne as it has its reservoirs in animals, via contaminated milk or meat
-> typical symptoms are abdominal pain, diarrhea, fever
transmission of bubonic plague -> from rodents to fleas to humans
typical symptoms of bubonic plague:
-> high fever
-> breathing constriction
-> opening of swollen buboes
-> seizures (Krämpfe)
-> extreme exhaustion
spiral shape allows to move through the mucous lining of the human stomach
its urease (enzyme) production enables it to survive in gastric acid (h.pylori-urease-test)
widespread; half of the population may carry the bacterium although not everybody develops a disease such as gastritis
transmission:
-> primarily by person-person through close contact
-> many remain asymptomatic, but linked to peptic ulcers (duodenum or stomach) or inflammation of stomach lining, which can lead to gastritis and increased risk of stomach cancer (long-term infection)
diagnosis & treatments:
-> endoscopy with taking samples of stomach lining
-> treatment with combination of antibiotics and acid reducing medications
prevention:
-> good food hygiene, safety of water and food sources
-> addressing potential risk factors such as crowded living
long flagellum
pathogenic agent is a toxin produced by bacteriophage, which affects the channels of epithelium, which usually keep balance of the extracellular fluid towards the tissue, so it’s blocking the channels entering the water
as toxin binds to the cell and is not able to move to another cell -> self-limiting disease (remember renewal of epithelial tissue within 48hrs)
main symptom is severe loss of fluid (really huge loss) and therefore really severe dehydration -> until lifethreatening stage
treatment therefore is only rehydration or oral or by additional infusions
dehydration leads to a number of severe side effects
natural source: brakish and salt water
-> therefore worldwide issue, but especially in those countries with poor hygenic conditions (central america, africa, india, china)
mycobacteria
characterized by a very specific cell wall
broad capsule, especially enriched with a number of proteins, which focus and build pores, where contact can occur between the inside (cytoplasm) and the outside of the cell
very complex and highly structured
-> long replication time!!!
=> very specific element of mycobacteria
mycobacterium tuberculosis
“old” bacterium from ancient times (such as myc lepromatosis) which didn’t became an epidemic stage before industrialization in 18th/19zh century -> many people crowded in poor living conditions
affected mainly young people (those where working in the industrialization process)
found by Robert Koch in 1882
requires oxygen to grow -> therefore high affiliation to the lungs!
nonmotile
divides only every 18-24 hours (therefore primary examination was difficult as cultures were hard to grow over weeks)
can easily survive for weeks without water, so still living after days; and transmission still possible!!!
quite resistant to desinfectants due to its high developed capsule -> to erase it from surfaces, intense desinfection is needed!
can not be identified with gram staining! (due to capsule and the whole strct) -> nowadays, analysis of antibodies (by staining of antibodies, which is available only since the late 20th century)
still spreading in a number of countries, and due to high motility (travelling), one can easily catch up the myc tub
95% of carriers are asymptomatic; more than 1/4 of world population carry the myc
not a problem with healthy IS -> additional risk factors: malnutrition, poverty, compromised IS
BCG vaccination exists, but only 20% decrease of risk, so not a routine anymore
onyl human-human transmission, and only with humans, who are in the stage of spreading the bacteria; which is not the case the whole time, but only with sneezing and coughing
-> prevention of spreading by isolation!
-> prevention by wearing a mask!
-> prevention by good, intense desinfection and general hygenic standards
-> pathology & pathophysiology
different stages (can be identified by x-ray examination):
-> latent infection: only small local activites, incapsulated process within the lungs
-> cavitary tuberculosis: highly infectious because of large cavities being formed due to distruction of lung tissue; bact can spread towards next person
-> miliary tuberculosis: with many little localisations, again not infectious; pure lung affected tuberculosis
=> PRIMARY TUBERCULOSIS
around most of the cavities or small spots, a healing fibrosis or calcification is formed, so surrounded by fibrous tissue or CT and can therefore not spread to neighbouring regions
-> effective tool of body to stop spreading (can be easily seen in xrays), but still living bact within these strcts!!!
-> reactivation is always possible, especially with additional issues, such as a decrease in IS fct (but also malnutrition and other stress factors), might allow the bacteria to reorganise, to leave the organised sheath and to enter the blood system (even after years!) where it can form a bacteriemia; but only 10% develop progressive primary tuberculosis
can affect a number of organs:
-> liver and spleen (mainly)
-> the joints and the long bones
-> the adrenal gland; causes hormonological disturbances
-> can lead to immunological problems
-> brain with meninges can be affected, too
-> immunological reaction:
1) macrophages in alveoli phagocyte myc tub, but as soon as inside, myc tub forms protein that inhibits interaction of macrophage with lysosome, why myc tub survives
2) a so called CASEATING GRANULOMA with involvement of neutrophil granulocytes -> problem, that bacteria are still alive and proliferate; if not calcified, which means, in this case bacteria are dead
-> two stages of IS system reaction:
depending on the stage, we have different antibodies, and therefore one can identify, if it’s active and in a fresh active form, or if it’s chronic
-> complicated, long-lasting treatment
mycobacterium lepromatosis
also known for a long time
quite an issue in middle ages
diagnosis possible by vision as skin and joints get affected
in the middle ages, affected people were excluded from social life and had to live in leprosories (poor and rich)
highly developed cell wall and capsule (as myc tub)
spreads human-human
high modern hygenic standards led to decrease in numbers nowadays
doubling time 12-14 days!!! -> cannot be cultured
-> takes a long time until syptoms manifest
myc lep is an intracellular parasite -> hard for IS to recognise
nowadays two hotspots -> india, brasil (big cities)
-> skin: pale or reddish lesions or nodules in different sizes
-> nervous system: numbness, which leads to secondary disturbances such as deformations of the hands and feet; hair loss due to interruption of innervation and cycle of the hair
incubation time 5 yrs!!! -> problem, as it is difficult to link showing symptoms to an infection with myc lep 5 yrs ago
treatment: in an early stage, antibiotic treatment quite effective
mycoplasma pneumonia
very exception of bacterium!!!
=> does not have a capsule AND no cell wall!
-> only double lipid layer membrane
small and very agile
adheres at the cell membrane or locates intracellular
-> in both cases it is difficult for IS to act against it
primarily in the respiratory tract, where it can climb inbetween the kinocilia
macrophages start inflammation in response to the bacteria -> pneumonia;
=> mycoplasma pneumonia can evade the response as it can enter the intracellular space and therefore resist the immunological response for a long time
=> can eventually spread within the body and lead to many non-specific symptoms:
headaches
loss of appetite -> can reach chronic stage, anorexia-like
mood swings; depression
infection of the heart with high heart rate
gastric symptoms such as vomiting and nausea
affection of bones and joints -> pain
treatment with antibiotics
spirochaetes
treponema pallidum
borreliose
leptospira
-> curled appearance due to high activity of axial filament
6-15 micrometers long, quite small but impressive length; highly curled
usually sexually transmitted bacterium -> syphillis
locally it is restricted to affect skin and bones
-> pinta (only skin)
-> bejel (includes bone)
-> yaws (includes bone)
-> classical infection
first three weeks after infection no symptoms (bacteria needs time to start to grow and to invade in the tissue)
primary syphillis -> local signs of skin affection: small lesions at the site where the contact with the other person has occured (sexual organs or e.g. mouth); often no pain, and therefore often overseen
primary signs will heal out by themselves; problematic as bacteria continue to live and to replicate in the body
silent period of up to 24 weeks
secondary syphillis with different signs: often dermal changes such as rash on the skin in various places (sole or back of the foot); accompanied by hepatitis, meningitis or glomerulonephritis
=> signs will heal out themselves, too
=> last longer than during primary syphillis -> longer time frame to recognize
=> if recognized has to be treated to stop further growth of treponema pallidum
=> if not recognized -> latent syphillis
latent syphillis can last 3 to 30 yrs; secondary syphillis can repeat; and if IS slows down, tertiary syphillis can occur
tertiary syphillis with GUMMA of skin -> more deep inflammatory reaction with destroying of the whole skin; most problematic part:
=> affects a number of organs, mainly the nervous system -> lead to a degeneration of the neurons and mimic of all types of CNS diseases
can be more global and appear like parkinson syndrome
can appear like tardis dorsalis
can appear like general dementia (so it can change the behaviour of the people
-> in this stage the bacteria are so widely distributed that it becomes difficult to perform effective treatment; and treatment is only stabilizing for no longer loss of fct (but if nervous cells started to degenerate, the degenerated aspects and parts can not be reestablished)
SECONDARY SYPHILLIS
-> mostly identified
-> dermal non-itchy rash
-> mucous lesions (condyloma latum)
-> non-specific symptoms: fever, sore throat, weight loss
-> 4-10 weeks after primary infection
-> symptoms resolve after 3-6 weeks
-> can be proofed serologically by drawing blood!!!
at every stage a single dose penicillin injected is sufficient!
condoms and abstinence most effective tools
CONGENITAL SYPHILLIS
infected women can transduce tre pa towards the fetus
-> deformations in the face, as saddle nose
-> changes in the teeth
-> other symptoms
=> has to be treated, otherwise newborns will suffer from bacteriosis and that shortens their life span
borrelia
zoonotic disease/infection (usually no human-human transmission) -> mostly infections occur in contact with ticks
first sign: typical rush with ring-like appearance growing from the center to the periphery
=> ERYTHEMA MIRGRANS
(while outer area grows, region where bacteria entered becomes normal again)
-> first sign usually followed by a stage of silence during which skin reaction passes away
secondary symptoms (occur months or even years later)
-> peripheral neuropathy
-> encephalopathy
-> fibromyalgia
-> psychic and neurologic symptoms
(neuroborreliosis)
problem: borrelia can enter the nerve cells
-> IS can no longer respond and pure immunologic clearance no longer possible
-> additional chemics/antibiotics neede, which can pass blood-brain-barrier
long-lasting therapy
not easy to check because of lacking of immunologic response which could be proofed by antibodies in the blood
enters the body and distributes in the whole body with variety of possible diseases and symptoms; non-specific reaction can occur in almost any organ
ACUTE PHASE (shortly after contact with the bact)
-> fever with headache as an affection of the brain
-> conjunctiva (eyes affected)
-> coughing (lungs affected)
-> abdominal pain and vomiting
-> pancreatitis
-> inflammation of liver and gallbladder
-> diarrhea (small or large intestine involved)
-> muscle pain
-> skin rash (rare event as leptospira is mainly seen
internal)
IMMUNE PHASE (when IS starts to act against the bacteria and starts inflammatory process)
-> meningitis (in sheath of brain)
->myocarditis (if heart is affected)
-> in the features of the GI tract
-> kidney failure…
enters the epidermis -> dermal disease
if skin has small breaches (Verletzungen)
-> can enter the tissue and towards the blood system and then can spread throughout the the different organ sites
well protected skin usually a sufficient barrier to avoid infection with leptospira
transmission from environment (not human-human)
bacterium lives in warm, humid conditions in the environment -> mainly at aquatorial zone, so very rare event in europe
Last changed6 months ago