5 important genera of gram positive rods:

1) Bacillus
2) clostridium
3) corynebacterium
4) Listeria
5) gardnella.
Bacillus and clostridium can form spores while others do not and bacil. And clost. Are longer and
deeply staining that others. COrynebacterium has V or L shape.

BACILLUS
2 types: bacillus anthracic and bacillus cereus
1) Anthracic
 Causes anthrax in animals, rare in humans
 In humans are: cutaneous, pulmorary and gastrointestinal

Properties:
 Large gram positive rod with square ends, found in chains
 Antyphagocytic capsule contains D_glutamate 9 non-motile)
 Anthrax toxin is encoded on one plasmid and polyglutamate capsule is encoded on a
different plasmid.

Transmission:
 Spores persist in soils.
 Humans are infected from trauma to the skin, or R tract.
 Pulmorary anthrax happens when spores are inhaled in lungs, Gastrointestinal occurs when
contaminated meat is ingested.
 Inhalation anthrax is is not communicable from person-to person. After inhaled into the
lungs it moves rapidly to the mediastinal lymph nodes, where causes hemmorragic
mediastitis.

Pathogenesis:
 Is based on 2 exotoxins: edema factor and lethal factor. Each contains A_B proteins
subunits configuration. A or active has enzymatic activity, while B for binding, has
protective function,\.
  Edema factor is adenylate cyclase that couses an increase in the intracellular concentration
of cyclic adenosine monophosphate, that couses outpouring of fluid from cell to
extracellular space, manifest as edema.
 Lethat factor is a Protease, cleaves phospohokinase, that activate mitogen-acticared
protein kinase that provides cell growth, protective antigen creates pores along membrane
that allows lethat and edema facto enter the cell.

Clinical findings:
 Lesionn of cutaneous anthrax is painless with black eschar ( crust,scab)
 Local is striking. The lesion called malignant pustule
 Pulmorary anthrax also called wool sorters disease, begins with R tract symptoms,
resembling influenza, dry cough, septic shock and death.
 Symptoms of gastrointestinal anthrax involves- vomiting, abdominal pain, bloody diarrhea.

Laboratory diagnosis:
- Using polymerase chain reaction ( pCR) based assays
- Another is serologic test such as enzyme linked immunosorbent essay ( ELISA)

Treatment:
- Ciprofloxacin and doxycycline
Prevention:
- Vaccine- BIOTHRAX, containing purified protective antigen as immunogen .

Bacillus cereus:
- Causes food poisoning.
- The spores germinate when rice is kept warm for many hours or reheated
fried rice
- Portal of entry is GI tract.
Pathogenesis:
 Produces 2 enterotoxins: Cholera toxin, it induce ADP-ribosylation-it adds adenosine
diphosphate ribose to a G-protein which stimulate adenylate cyclease, leads to increase
concentration cyclic AMP within enterocyte.

Clinical findings:
 2 symdromes: 1) has short incubation period ( 4 hours ) consists nausea and vomiting
( similar sthapylococcus) 2) has long inc. period ( 18 hours) features watery nonbloody
diarrhea, resembling clostridial gastroenteritis.
Clostridium:
 4 medially important species: tetani, botulinum, perfringens ( couses gas
gangrene or food poisoning) and difficile.
 All are anaerobic, spore-forming

1) Clostridium tetani
 Spores are widespread in soil, portal of entry is wound site,, or during “skin poping” ,
technique used to inject drugs into skin.
 Pathogenesis: Tetanus toxin- tetanospasmin produced by vegetative cells, is carried to the
central nervous system, where it binds ganglioside receptors and blocks release of
inhibitory mediators. ( glycin or Gaba) at spinal synapses.
 Tetatus and botulinum toxin are most known, both proteases, cleave proteins involved in
mediator release from neurons.
 Tetanus is antigenic type. Tetanus toxoid is against tetanus.
Clinical findings:

 Tetanus characterized by strong muscle spasm ( spastic paralysis), features- lockjaws due to
rigit contraction of jaw muscle, which prevents mouth to open, known as Risus Sardonicus.
 Opisthotones – arching of the back muscle, due to spasm of extensor muscle of the back
 In Tetanus- plastic paralysis, whereas in botulism- Flaccid paralysis

Laboratory diagnosis:
 Clostridium tetani produces terminal spores, that gives feature of Tennis racket.

Treatment:
 Tetanus immune globin is used to neutralize the toxin.
 Antibiotics are: metronidazole, penicillin G., benzodiazepins given to prevent spasm.

Prevention:
 Prevented by immunization with tetanus toxoid, given children in combination with
diphtheria toxoid and acellular pertussis vaccine.
 When trauma occurs wound shoud be cleaned, and tetanur booster should be given and
penicillin administered.
 The administration of both, immune globulins and tetanus toxoid are example of passive
activity immunity.
 Clostridium botulinum:
Causes botulism.
 Spores widespread in soil, contaminate vegetables and meats.
 Spores can survive in anaerobic environment
 Highest risk food are: 1) alkaline vegetables ( beans, peppers, and muchrooms)
2) smoked fish. ( can inhibited by sufficient boiling)
Pathogenesis:
 Botulinum toxin is absorbed from gut and carried via blood to peripheral nerve
synapses, where blocks release of acetylcholine
 There are 8 immunologyc types: A,B and E are most common.
Clinical findings:
 Descending weakness and paralysis of cranial nerves including diplopia,
dysphagia, ptosis and Resp, muscle failure, no fever in contrast to Guallim-
Baare syndrome –ascending paralysis.
 2 special clinical forms occur: 1. Would botulism at site 2. Infant botulism in
gut.
Laboratory diagnosis:
 Enzyme-linked imunnoassay to detect toxin, PCR to detect DNA
Treatment:
 Heptavalent antitoxin: 7 types A-G.. antitoxin made in horses and serum
sickness may occur. Type A and B from plasma
Prevention:
 Proper sterilization and vacuum packed foods is essential.

3. Clostridium perfringens:
 Causes 2 disease: gas gangrene and food poisoning
Gas gangrene: caused by C perfringens, streptococcus pyogens, staphylococcus
aureus, (myonecrosis, necrotizingm, fasciitis) necrotizing fasciitis also called “flesh-
eating’’
Transmission: spores are in soil, vegetative cells are members of the normal flora of
the colon and vagina
Pathogenesis:organisms grow in traumatized tissue and produce varienty of toxins,
most important is alpha toxin, that damages cell membranes of RBD, resulting
hemolysis.

Clinical findings: Pain, EDEMA, cellulitis, and gangrene. If crepitus is palpated in the
affected area it indicated gas in tissue. Can occur hemolysis, endometritis, shock and
death.
Laboratory diagnosis: organisms are cultured anaerobically and then identified by
sugar fermentation reactions and organic acid production.
Treatment: penicillin G.
Food poisoning- caused by c perfringens, spores are located in soil and can
contaminate food. The heat resistant spores survive cooking and germinate. The
organism grow to large numbers in reheated foods, especially meat dishes
Pathogenesis- entetotoxin cause diarrhea. Act as superantigen.
Clinical findings: has 14-16 inc. period

4. Clostridium difficle:
 Causes amtibiotic associated pseudomembranous colitis, is the most common
nosocomial cause of diarrhea.
Transmission:the organism colonizes the large intestine by fecal-oral route,
majority occur hospitalized patients.
Pathogenesis:exotoxins causes depolarization of actin resulting loss of
cytoskeletal integrity, apoptosis and RBC death.
Clinical findings: causes diarrhea, associated with pseudomembranes on the
colonic mucosa. The organism rarely enters the bloodstream and rarely couses
metastatic infections
Laboratory diagnosis: 2 types test: one detects exotoxins and other detect the
exotoxins itself and the other detect the genes that encode the exotoxins.
Used elisa and PCR assay.
 Trearment:oral metronidazole or vankomycine
Prevention: no prevention vaccines.

Non-spore forming Gram-positive RODS:

3 important pathogens: Corynebacterium, diphteriae, Listeria monocytogenes,
Gardnella vaginalis

1) Corynebacterium diphteriae
 Causes diphtheria
 Are gram positive rods, appear club-shaped, arranged in V or L shaped
formations, rods has beaded appearance, has granules, highly polymerized for
storage of energy. Stain metachromatically.

Transmission: are in upper respiratory tract, transmitted by Airbone droplets, organism

can infect the skin

Pathogenesis: diphtheria toxin inhibits ADP-ribosylation of elongation factor-2. Toxin has single
polypeptide with A_B domains. A or active posses enzymatic activity, while B for binding.

Corynebacterium cells don’t produce exotoxin and are nonpathogenic.

HOST response:

 Local inflammation in the throat

 Antibody that can neutralize exotoxin activity by blocking the interaction of
the binding domain with the receptors, preventing entry into the cell.
 Immune status of a person can be assessed by Schick’s test, performed by
intradermal injection, if person hasn’t antitoxin, the toxin cause inflammation
at the site 4-7 days later.
Clinical findings: Pseudomembrane over the tonsils and throat, fever, sore throat,
cervical adenophathy. 3 prominent complications:
 Extension of the membrane into the larynx and trachea, cause airway
obstruction
 Myocarditis accompanied by circulatory collapse.
 Nerve weakness of paralysis ( esp. Cranial nerves)
 Cutaneous diphtheria causes ulcerating skill, covered by gray membrane.
Laboratory diagnosis: involves both: isolating the organism and demonstating toxin production.
Tellurite plate and a blood agar is used. Tellurite plate contains tellurium within the organism.

Treatment: antitoxi, can neutralization, Also Penicilin G or erythromycin.

Prevention: treating the exotoxin with formaldehyde that inactivates toxic effect.

LISteria monocytogenes:
Causes meningitis and sepsis, outbreaks of fexrile gastroentrities.
Properties: small, arranged in V or L shaped, motile, grows well at cold temperature
 Pathogenesis: occurs in fetus or newborn across the placenta or during
delivery, or in pregnant women and immunosuppressed adult. The organism
is distributed worldwide in animals, plants, soil and can transmit to humans
 Pathogenesis is depend on the organisms ability to invade and survive within
cells, has ability to cross placenta and invade GI tract.
 When entering the cell, organism produces listeriolysin, allows it to escape
from phagosome into the cytoplasm
 Listoria monocytogens can move from cell-to cell, by actin rockets.
Clinical findings: during pregnancy can abortion, sepsis, meningitis 1 to 4 weeks later.
Gastoenterities caused by L monocytogenes is characterized by watery diarrhea,
fever, headache.
Laboratory diagnosis: made by gram stain and culture. The isolation of listeria is
confirmed by the presence of motile organisms, which differenciate them from
nonmotile corynebacterium.
Treatment: ampicillin and Trimethoprimsulfamethoxazole, Listeria doesn’t require
treatment.
Preventon: difficult because there is no immunization

Gardanella vaginallis:
 Associated with bacterial vaginosis, vaginal infection of sexually active women.
 Properties: small gram-variable rod, means that some are purple, while others
are pink, structurally has gram-positive cell wall, but the wall is thin and tend
to lose purple color
 Pathogenesis: GArdanella vaginalis often found associated with anaerobs such
as: mobiluncus and prevotella and non-araerobs such as mycoplasma
hominies and ureaplasma urealyticum.
 Is not transmitted by sexually, normal flora of vagina are replaced by those
organisms.
 Clinical findings: Bacterial vaginosis is characterized by malodorous, white of
gray-colored, mild itching may occur.
 Laboratory diagnosis: Clue cells which are vaginal epithelial cells are covered
by bacteria, are laboratory findings. Also Whitt test or PH of greater than 4.5
of the vaginal discharge indicates diagnosis of bacterial vaginosis
 Treatment and prevention: drug is metronidazole, no vaccine.