Microbiology bacteria summary Gram +ve

Genus Staphylococcus

Species Aureus (coagulase +ve)

Description Anerobic Non-sporing Non-motile Non-capsulate / limited capsule formation Catalse +ve Appear as bunches of grapes

Cocci aerobic Virulence factors & Pathogenesis Enterotoxins - food poisoning - heat stable -Toxic shock syndrome toxin (TSST-1) Epidermolytic toxins - type A&B - cause blistering disease cytotoxin alpha toxin - pore formation - proinflammatory protein A - disrupts opsonization - binds IgG in Fc region (bind Ig with irregular orientation to disrupt opsonization) Causes infection of sites of lowered resistance damaged skin / mucous membrane Enterotoxin & TSST-1 = superantigens - activate T lymphocytes - release cytokines (TNF) coagulase & bound coagulase (clumping factor) Nuclease Haemolysans leukocidins

Epidemiology Nose of 30% of healthy people Skin, glands and mucous membranes Colonization: - nares, axilla, vagina, pharynx

Diseases Skin infection Osteomyelitis Food poisoning

Treatment Inherently sensitive to many antimicrobial agents 90% resistant to: penicillin G (benzylpenicilli n) resitance via: -lactamase (penicillinase) antibiotics: - must use lactamase resistant penicillins - cloxacillin - flucloxacillin MRSA (Methicillinresistant Staph. aureus) use vancomycin

epidermidis Coagulase ve

Normal flora of cutaneous organ system

Adhesion to biomaterials - adhesion to silastic catheter by capsular polysaccharide adhesion - forms biofilms via extracellular slime substance

Major cause of foreign body infection

resitance via: -lactamase - vancomycin

Streptococcus

Pyogenes (pus forming) aka group A streptococcus GAS (Lancefield grouping) haemolysin

Facultative anaerobe: - makes ATP by normal aerobic respiration - ferments in absence of O2 Non-sporing Non-motile capsulated Catalase ve

M proteins - prevent opsonization by C3b - B cells can produce anti-M protein Ab Ab also damages cardiac muscles rheumatic fever Toxins - superantigens do not require processing by APC - bind directly to T cell MHC II (nonspecificly) huge cytokine release - rapid onset - pyrogenic - toxic onset syndrome super bug / flesh eating bacteria capsule-hyaluronic acid - antiphagocytic haemolysins streptolysins O & S - lyse: eryhtrocytes, leucocytes, platelets - -haemolysis hyalournidase - degrades hyaluronic acid of ground substance streptokinase - fibrinolysis spreading DNAases localized infections suppurative infections (pus forming)

Pharyngitis Skin infections Rheumatic fever - type 2 hypersensitivity acute glomerulonepgr itis - immune complex deposition in glmoeruli

Penicillin still effective for Goup A streptococcal antibiotics: - penicillin G & V Specific Mprotein vaccines being tested typing: - -haemolysis +ve = pathogenic clear zone around colony in blood agar - -haemolysis = mostly commensals green for oxidation by hydrogen peroxide (not actual haemolysis)

Pneumoniae (pneumococc us) haemolysin optochin sensitive Viridians (green) haemolysin optochin resistant Commensals

Pneumonia Meningitis in children and adults

Typing: - -haemolysis

Genus Peptostreptococ cus

Species

Description Anaerobic Non-sporing

Cocci anaerobic Virulence factors & Pathogenesis Normal flora of skin, oral cavity, colon, genitourinary tract

Epidemiology 1. Abscesses: - brain - lung 2. Aspiration pneumonia 3. Gingivitis + other periodontal diseases

Diseases

Treatment

Genus Listeria

Species Monocytogene s

Description Intracellular pathogen

Bacilli aerobic Virulence factors & Pathogenesis Found in environment and animals Contaminates food Humans = local carriers

Epidemiology Adults: - asymptomatic GIT carrier - influenza like

Diseases

Treatment antibiotics: - penicillin Prolonged ampicillin -lactamase inhibitor: - clavulanic acid Resistant: - cephalosporins (intrinsically)

Genus Clostridium

Species Tetani

Description Anaerobic sporing

Bacilli anaerobic Virulence factors & Pathogenesis Toxins: tetanospasmin - neurotoxin very leathal - blocks neurotransmitter release for 3-4 days enzymes: - oxygen-labile haemolysin (tetanolysin) Spread: 1. ascending tetanus wound to trunk via pheripheral nerves 2. Descending Haematogenous via lymp = lock jay

Epidemiology Found in soil & animal feces spores enter deep tissue with low oxygen tension

Diseases 1. Tetanus - vascillating spasms - respiratory arrest - death if dose is high

Treatment Diagnosis: - smear from lesion Immunization: - active tetanus toxoid (neutralize unbound toxin) - passive immunoglobulins Supportive: - mechanical ventilation - muscle relaxants - sedation - nutrition antibiotics: - metronidazole (kills vegetative bacteria) - penicillin G & V Vaccine: - toxoid vaccine helps clear unbound toxin if given immediately BUT questionable efficacy Antibiotics: - penicillin supportive care

Botulium

anaerobic Sporing

Toxins: 1. neurotoxins - 7 forms (A-G) - invasion of peripheral nerves blocks release of Ach flaccid paralysis ocular and respiratory muscles - blurred vision - trouble swallowing

Highly resistant spores Found in feces, blood, food

Perfringens

Anaerobic sporing

Toxins: exotoxins - deep tissue necrosis - gas production causing crepitus

1. Clostridial myonecrosis gas gangrene - complications shock, haemolysis, renal failure, metabolic acidosis, coma 2. Enteric infection -food poisoning - enteritis necrosis - neutropenic enterocolitis 3. Soft tissue infections - polymicrobial infection - crepitant cellulitis - suppurative myositis

- Extensive debridement - possible amputation antibiotics: - penicillin G & V sometimes hyperbaric O2

Difficile

Anaerobic sporing

Toxins: - Enterotoxin - cytotoxin Antibiotics kills many GIT flora other than difficile multiplies and produces toxins complications: - hypoproteinaemia -toxic colonic perforation - peritonitis

Part of normal GIT flora in many individuals

1. Antibioticassociated diarrhoea + pseudomembrano us colitis watery blood diarrhoea 4-9 days post antibiotics

Discontinue antibiotic supportive: - rehydrate avoid anti-motility drugs antibiotics: - metronidazole - vancomycin (if severe)

Propionibacteri um

Normal flora of the skin Opportunistic infections: - prosthetic devices - CNS shunts

Bifidobacteriu m Eubacterium

Questionable pathogenic potential

- Predisposing condition - dental extraction Female genital tract - ICUD (contraceptive) Predisposing condition

Chronic periodontal disease

Actinomycetes

Israelii

Actinomycosis - chronic, granulomatous infective disease - multiple abscesses, sinus tracts, fistulae erupt to the surface drain pus containing sulphur granules

Antibiotics: long course penicillin

Gram ve

Genus Neisseria (described by Neisser)

Species meningitidis

Description Obligate human pathogens Diplococci (axis of pair parallel side by side) Oval cocci to bean shaped Found inside neutrophils (polymorphonucl ear pus cells) Capsule (determines serogroup)

Cocci - aerobic Virulence factors & Pathogenesis Immune evasion via capsule Bacteremia Antibodies and complement are essential for host immune response

Epidemiology Carriers in: nasopharynx oropharynx Increased incidence in winter Spread by kissing Spread via respiratory droplets

Diseases Meningococcal meningitis Danger of major out break -endemic & epidemic situations 2/3 of cases under age of 5

Treatment Vaccine preventable (based on capsule serogroups) - last 3 years -immunityprophylaxis - herd immunity vaccinate population groups to avoid outbreaks catch early treat early - chemoprophylaxis - if danger of outbreak treatment should begin before definite diagnosis - notifiable Antibiotics: - penicillin G & V

gonococcus

Non-capsule

Pili (phase variation)

Antibiotics: - penicillin G & V

Genus Veillonella

Species

Description

Cocci anaerobic Virulence factors & Pathogenesis

Epidemiology often contaminates skin commensal of: - mouth, upper RT, GIT, vagina

Diseases 1. Osteomyelitis 2. Periodontitis

Treatment 1. antibiotics 2. Surgery - incision, drainage, debridement, removal of foreign bodies 3. Improve circulation oxygen

Genus

Species

Description

Bacilli aerobic Virulence factors & Epidemiology Pathogenesis

Diseases

Treatment

Enterobacteria Escherichi a Coli ? strains EPEC enteropathogeni c ETEC Enterotoxogenic Aerobic (use / ferment carbohydrates) GIT commensals ? Found in: soil, plants water Adherent bacteria Adheres to gut wall (upper intestine) - loss of microvilli water & electrolyte absorption Toxins 1. fimbriae adherence to epithelial membrane of small intestine 2. enterotoxins - heat stable and heat labile - hyper secretion of fluids and electrolytes in to lumen EIEC enteroinvasive Invasive bacteria Direct penetration, invasion and destruction of intestinal mucosa Toxins Cytotoxins - VT1 - VT2 Common in tropics - bad hygiene Infantile diarrhoea - mild fever, malaise, vomiting - large amount of mucous in stool no blood Diarrhoea in adults and infants travelers diarrhoea Major cause of death in children <5 rapid onset no blood 1-5 days Dysentery - scanty stool with pus, mucous, blood Fever, abdominal cramps, malaise Severe in old and young hemorrhagic: - diarrhoea - colitis - uremic syndrome (HUS) platelets, hemolytic anaemia, renal failure no leukocytes in stool Fever, abdominal cramps Chronic diarrhoea (malnourished children) Colonized but not pathogenic Supportive - replacement of water & electrolytes avoid exposure to infecting agent - boil it, peel it, or leave it no antibiotic treatment recommended - diarrhoea normally self-limiting in VTEC - antibiotics associated with development of HUS antimicrobial prophylaxis not advised development of resistance

Tropical and subtropical climates Contaminated food and water Poor sanitation

Food borne Out breaks in schools and hospitals for the mentally handicapped Out breaks - nursing homes - day care centres food - hamburger meat, cooked meat - unpasteurized milk

VTEC Verocytotoxioge nic (aka enterohaemorra gic)

EAggEC enteroaggregative

Adherent bacteria Adheres to mucosal surface of intestine

Rare in industrialized country

Shigella

Dysenteriae (serogroup A) Closely related to Escherichia

Non-motile non-capsulate

Invasive bacteria: Superficial invasion of the gut Toxin: Shiga Toxin - destroys epithelial cells - necrosis - neurotoxic - meningism (triad of nuchal rigidity [stiff neck], photophobia, headache) - coma Toxin Enterotoxin Non-invasive

Transmission: - human to human - low infective dose 10 viable bacteria 4 Fs: Fingers Faeces Flies Food No animal reservoir Outbreaks / epidemics Contaminated water

Most common in children Dysentery: - Bloody diarrhoea Bacteraemia = rare

-lactamase inhibitor: - clavulanic acid

Vibrio

Cholerae

Watery diarrhoea (20-30 liters/day) Rapid onset Hypovolemic shock Metabolic acidosis Cyanotic sunken eyes and cheeks Poor skin tugor

Detection: - fresh fecal sample 1-2hours - rectal swab vaccine: - given to groups in high risk areas Dukoral: - 85-90% efficiency - all ages - for 4-6 months

Parahaemolyticu s

Acquired from food - mainly raw seafood

Dysentery-like picture

Salmonella

Enterica typhi Non-typhi

Aerobic non-sporing rods (coccobacillus) motile

Enter macrophages?? 1. primary bacteraemic phase: Invades ileal mucosa multiplies in mesenteric lymphoid tissue enters blood via thoracic duct liver, gall bladder, spleen, kidneys and bone marrow become infected

Fever: - enteric fever - typhoid fever (if causative agent is typhi) long term asymptomatic carriers: - chronic excretion - biliary necrotizing cholecystitis - urinary tact - dangerous for food handlers to be carriers Diarrhoea found in: - CSF - Stool, urine, blood

Detection: Blood cultures ESBLproducing salmonella Vaccine: - live attenuated Ty21a approved for travelers

-lactamase inhibitor: - clavulanic acid

2. Second (heavier) bacteraemic phase: 7-10 day incubation period conincides with fever 3. Further infection of GIT from gall bladder Preyers patches and lymphoid tissue involved inflammatory response typhoid ulcers

Transmission: - human to human

Genus Bacteroides Porphyromon as Prevotella Fusobacteriu m

Species Fragilis

Description

Bacilli anaerobic Virulence factors & Pathogenesis

Epidemiology Normal flora: oral cavity, GIT, vagina

Diseases 1. abscess formation 2. Periodontal disease - Vincents angina acute necrotizing ulcerative gingervitis 3. post aspiration pleuropulmonary disease 4. Genital tract infections

Treatment 1. antibiotics 2. Surgery - incision, drainage, debridement, removal of foreign bodies 3. Improve circulation oxygen

Genus

Species

Description

Rods (coccobacilli) Virulence factors & Pathogenesis

Epidemiology

Diseases

Treatment

Nosocomial infections Pseudomonas Aeruginosa Rods (coccobacilli) Non enterobacterica cea Non-fastidious (simple nutritional needs) Ubiquitous in nature opportunistic, nosocomial pathogens Obligate aerobic capsulate (mucoid polysacch aride) glucose oxidizer Toxins: - exotoxins A - lipopolysaccharide Enzymes: - protease - phospholipase C Invasins: - elastase - hemolysins - cytotoxin - pyocyanin Adhesins: - pili - alginate capsule-biofilm Genetic attributes: - transduction, conjugation, antimicrobial resistance Opportunistic pathogen Can infect almost all tissue Systemic infections in compromised patients can be 50% fatality rate Survives in: - hydrotherapy baths - hot tubs - swimming pools Can infect all tissues oppertunisitc pathogen - systemic infection in compromised host 50% fatality rate Resistance: - high [] of salts and anti-septics antibiotics: - piperacillin (ureidopenicil lins) + tazobactam ( -lactamase inhibitors)

4-42C

Acinetobacter akinetos = unable to move Bactrim = rod

Baumannii

Aerobic Nonmotile 20-30C

- Attachment - persistence on surfaces - secretion of enzymes and toxins

Enters via: - open wounds - catheters - breathing tubes - Fomites - contaminated parentral solutions pathogen amongst wounded soldiers moist and dry conditions normal flora of oropharynx of some hosts colonizes: - skin, wounds, GIT, resp. tact Colonizes fluids in hospital settings

Resistance: - resistant to all available drugs for therapy

Stenotrophomo nas stenos = narrow trophos = who feeds monas = a unit

Maltophilia malt + philos = friend of malt

Low virulence Opportunistic pathogen rarely a true pathogen on its own

1. Nosocomial pneumonia 2. Present in many cystic fibrosis patients

Resistance: - lactams aminoglycosi des - inherent to carbapenems

Genus Fastidious Pasturella

Species

Description

Bacilli Virulence factors & Pathogenesis

Epidemiology

Diseases

Treatment

Multocida

Fastidious

Colonizes mucous membranes, upper resp. tract and GIT of mammals and birds Transmission: - bites and scratches

1. Localized infection from scratch 2. resp. tract infection 3. Systemic disease (life threatening) - meningitis - bacteremia

Antibiotics: - penicillin

Legionella

pneumophilia

Ubiquitous Transmission: - inhalation of aerosols

1. Legionnaires disease = febrile disease (associated with fever) + pneumonia + extrapulmonary involvement 2. Pontiac fever = without pulmonary involvement 3. Asymptomatic infection

Antibiotics: - quinolones (ciprofloxacin, ofloxacin) - macrolides

Haemophilus

Influenzae

Capsulate (serotype B) non-motile Catalase +ve oxidase +ve Fastidious Can be bacilli to coccobacilli pleomorphic Obligate human parasite Capsule: - 6 serotypes - serotype B most common enzymes: - IgA proteases

10% of upper respiratory tract flora Growth = 5-10% CO2 Transmission: - repertory drops entrance: - mucous membranes

Systemic: (encapsulated strains) - acute epiglottis - laryngotracheal infection - cellulitis / arthritis - pneumonia - septicemia - conjunctivitis local: (unencasulated non typable) - otitis media -sinusitis - pneumonia - bronchitis

Lab cultures: Requires - X factor haemin/haematin(blood) - V factor NAD (nicotinamide-adenine dinucleotide) from S. aureus -lactamase inhibitor: - clavulanic acid adjunctive medication: - steroids Resistance: - ampicillin (penicillin) vaccine: - HiB serotype B 1. endocarditis - long duration of symptoms large vegetations with potential to embolise 2. Skin and soft tissue infections 3. Eye keratitis, corneal ulcers Antibiotics: - penicillin

HACEK group Haemophilus Actinobacillus Cardiobaterium Eikenella Kingella aphrophilus actionomycet emcomitans hominis corrodens kingae

Fastidious

Found in human oral cavity

Diarrhoeal pathogens
1. Ingestion of preformed toxins
Clostridium botulinum Clostridium perfringens Staphylococcus aureus Bacillus cereus

Clinical: - Usually watery diarrhoea (water + electrolytes)

2. Toxins produced in the gut

Vibrio cholerae ETEC Clostridium difficile Aeromonas sp.

Clinical: - Usually watery diarrhoea - Bacteria &/ toxins found in stool

3. Invasive bacteria
salmonella shigella VTEC (aka EHEC) EIEC Yersinia enterocolitica Vibrio parahaemolyticus Clostridium difficile

Clinical: - dysentery / inflammatory diarrhoea - leukocytes (pus) & erythrocytes (blood) usually found in stool

4. adherent bacteria
EPEC EAEC

Clinical: - mucous diarrhoea

nosocomial infection
Infection Catheter-associated bacteruria Intravenous line infection Urosepsis Primary bacteremia Pseudobacteremia Predisposing factors Indwelling urinary catheter Central intravenous catheter Urinary tract instrumentation Arterial monitoring devices Contamination of blood during collection / processing of blood culture

Anaerobic infection
Ubiquitous in nature and commensals of GIT Weak pathogens ?? Produce toxins Cause polymicrobial infections

Clinical: - foul smelling discharge / odour - abscesses, necrotic tissue, gangrene - large quantity of gas production in tissue creptitus (crackling & popping sounds/sensation under skin/joints) - black discolouration of tissue - sulphur granules - blood in exudate situation suggestive: - bite wound infected - previous antimicrobial therapy - gram stained tissue yields organisms but no growth on culture treatment - antimicrobial therapy - surgery incision, drainage, debridement, removal of foreign bodies - improve circulation oxygen