Other Gram Negative Rods

Vibrio

this genus contains important intestinal pathogens of man, such as cholerae, which causes epidemic Asiatic cholera

Vibrio cholerae (strain El Tor)

milder form of disease, patients can be asymptomatic
bacteria survives in the body longer than classical strains: allows carriers to infect a greater number of people in the population
responsible for most cholera cases globally
biotype that caused cholera in Haiti after 2010 earthquake

Vibrio cholerae (classical)

relatively rare globally except in India and Bangladesh

man

the only host to Vibrio cholerae

convalescent carrier

those recovering from disease who shed bacteria for up to a year

chronic carrier

those who no longer ave disease but still carry bacteria for years

gall bladder

where do chronic carriers store bacteria

fecal-oral route

vibrio cholerae transmission route

oysters

what raw food is associated with Vibrio cholerae

enterotoxin

vibro cholerae pathogenesis
bacteria produce powerful enterotoxin which acts on the intestinal lining causing massive fluid and electrolyte loss
causes the pathogenic condition not the bacteria itself

vibrio cholerae complication

result from massive loss of essential electrolytes
hypovolemic shock
metabolic acidosis
mortality of untreated cases ~50%
mortality for treated cases <1%

Vibrio cholerae immunity

after resolution of infection, immunity is long-lasting for most people

Vibrio cholerae prevention

single dose vaccines are available for travelers to area where cholera is common
oral cholera vaccine (OCV) is available to prevent disease spread

children

what population does the OCV have limited protection in

vibrio cholerae treatment

fluid and electrolyte management
antibiotics such as tetracycline (to eliminate carrier state)

Vibrio cholerae

gram negative rod, comma-shaped
growth on simple culture/agar; or media specific for this is also available
oxidase positive
lactose negative

Campylobacter jejuni source

lower animals, such as dogs and cats
birds carry without becoming ill

Campylobacter jejuni transmission

ingestion of food such as poultry and unpasteurized dairy products as well as contaminated H2O
Associated with handling raw poultry

reserviors for Campylobacter jejuni

GI tract of chickens
water supply

Campylobacter jejuni symptoms

2-10 day incubation period
infection usually leads to fever, cramps, bloody diarrhea
blood diarrhea indicates the bacteria as an invasive pathogen that infiltrates the lining of the intestine
ulceration
self-limiting

erythromycin

Campylobacter jejuni treatment

Helicobacter pylori

leading cause of peptic ulcers and chronic gastritis

Helicobacter pylori source

more than 50% of the population globally harbors this in the upper GI tract

Helicobacter pylori transmission

person-to-person
fecal contamination of food/water

Helicobacter pylori manifestations

most infected people never suffer symptoms
it is common in countries such as Colombia and Chine where this bacteria infects over half the population in early childhood
some adults and children suffer from chronic active and persistent gastritis
long-term infection leads to a 2-6 fold increased risk of developing gastric cancer and mucosal-associated lymphoid tissue (MALT) lymphoma.

Endoscopy

what retrieval method is used for Helicobacter pylori

biopsy urease test

colorimetric test based on ability of Helicobacter pylori to produce urease
rapid test result of tissue from biopsy

histologic stain of tissue and culture

to identify the Helicobacter pylori present in the tissue 
this is the gold standard of diagnostic tests

urea breath test

Helicobacter pylori clinical diagnosis
patient is given either 14C labeled urea to drink
Helicobacter pylori metabolizes the urea rapidly and labeled carbon is released
labeled carbon is measures, usually as 14CO2, in the patient’s expelled breath to determine whether Helicobacter pylori is present

serum antibody test

Helicobacter pylori clinical diagnosis
determines if a person has been infected
if Ab are present, then the person has or had the infection

stool antigen test

Helicobacter pylori clinical diagnosis
antigen detection in stool samples:accurate, noninvasive test for direct dectection of Helicobacter pylori in stools
antigen detection equals active infection
not the definitive test of choice for diagnosis and treatment monitoring

Amoxicillin and tetracycline

antibotics effective against Helicobacter pylori

Helicobacter pylori treatment

antacid or proton pump
help alleviate ulcer-related symptoms
heal gastric mucosal inflammation

Campylobacter/Helicobacter

gram negative rods, curved and S-shaped
no growth on blood or MAC
microaerophilic: requires high CO2 environment to grow
Temperature preference: 42C
Biochemical ID: nonfermentive, oxidase positive, catalase positive

Pseudomonas

found in soil, water as natural habitat - is widespread in nature

Pseudomonas aeruginosa

aerobic Gram negative rods
nonfementative
most frequently isolated nonfermenter in clinical setting
producer of pigments

pyocyan

Pseudomonas aeruginosa pigment
characteristic blue-green color
fluorescent under UV light
occurs in vitro and in vivo

proteases

Pseudomonas aeruginosa determinants of pathogenicity
proteolytic necrotizing enzymes: hemorrhagic tissue destruction
corneal tissue destruction in eye infections

pyocyan

Pseudomonas aeruginosa determinants of pathogenicity
acts as toxin
kills competing microbes
generates reactive oxygen species 
inactivates catalase
interferes with electron transport chain

Exotoxin A

Pseudomonas aeruginosa determinants of pathogenicity
necrotizing activity at site of colonization

hemolysins

Pseudomonas aeruginosa determinants of pathogenicity
contribute to invasiveness, especially in pneumonia

Pseudomonas aeruginosa transmission

contaminated equipment
hospital personnel

people prone to Pseudomonas aeruginosa infection

occurs in people with altered host defenses such as
burn patients
patients with malignant diseases
patients receiving interventional treatments 

lesions or septicemia

Pseudomonas aeruginosa clinical infection
lesions may spread via the blood stream causeing septicemia with high mortality
localized lesions may occur in burns, wounds, corneal tissue, lungs, urinary tract

eye infections

Pseudomonas aeruginosa clinical infection
infection of corneal tissue may result in loss of vision in the eye

Leukemia Patients

Pseudomonas aeruginosa clinical infection
Pseudomonas aeruginosa is the 2nd most common cause of septicemia in these patients
the major defense they have is their innate immune system (phagocytosis)

Antibiotic resistance of Pseudomonas aeruginosa

intrinsic resistance to many antibiotics and acquired resistance to some
because of this resistance, it becomes the dominant organism present in the diseased area after other microbes are eliminated by the antimicrobial therapy
when infection is localized and external, treatment with topical antimicrobics, such as polymyxin B or colistin, is effective
if much necrotic tissue is present, it must be debrided befor topical treatment is effective
abscesses must be drained

Topical

Treatment oif Pseudomonas aeruginosa for burns, wounds, and eyes

Systemic by ingestion or injection

Treatment oif Pseudomonas aeruginosa for systemic infections

heptavalent vaccine

prevention of pseudomonas aeruginosa
developed for burn patients
proven effective in lessening incidence of infecition

Burkholderia pseudomallei

responsibole for life threatening human disease, Melioidosis (Whitmore’s disease), which is characterized by pneumonia and multiple abscesses and mortality rate of 40% 

Burkholderia pseudomallei

bacterium found in hte soil and water in tropical areas of Southeast asia
Vietnam war veterans had exposure to this microe, probably due to ectensive exposure to wet soils and surface water

high risk groups for Burkholderia pseudomallei

rice farmers, laborers, indigenous groups and adventure travelers to locations such as:
Veitnam
Thailand
northern Australia
Mexico

Burkholderia pseudomallei disease presentation

infection where an abscess forms and leads to aggressive granulomatous disease is caused by: ingestion or inhalation of contaminated dust, soil contamination of abraded skin
further abscess formation in lungs and other viscera
overwhelming and rapidly fatal septicemia can occure
chronic course resembles: tuberculosis with pneumonia, multiple abscesses, osteomyelitis

Hemophilus

small gram negative rods
characterizd by a requirement for specific grwoth factors that are found in blood

Hemophilus influenzae clinical infection

upper adn lower respiratory tract infections
pharyngitis
otitis media
sinusitis
pneumonia after descending into the lower respiratory tract

Meningitis

Hemophilus influenzae clinical infection
most serious disease produced by this bacteria: acute non-epidemic bacterial 
occurs in children from 3 months-6 years of age: elderly individuals are also susceptible

immunity

Hemophilus influenzae clinical infection: meningitis
transplacental for infants ages birth-6 weeks after which time natural immunity may begin to develop

Acute Bacterial Epiglottitis

Hemophilus influenzae clinical infection
occurs mostly in children between 2-7 years of age
infected epiglottis becomes swollen - may lead to closing off the airway which necessitates tracheotomy
septicemia may develop and be fatal

Hemophilus influenzae treatment

ampicillin and chloramphenicol are the most commonly prescribed

Hemophilus influenzae prevention

necessary because type B (Hib)
is an important cause of childhood meningitis
is a cause of bacterial pneumonia in children
is estimated cause of 3 million cases annually
is resistant to phagocytosis by alveolar macrophages, probably because it is encapsulated
several differed Hib vaccines are on the market
these vaccines are now part of routine childhood vaccination programs in more than 20 countries including the USA

Hemophilus influenzae laboratory diagnostics

requires nutritional factors directly supplies by chocolate agar
V factor (NAD)
X factor (Hemin)
Latex agglunination

Hemophilus aegyptius differentiation

needs to be differentiatied from H. influenzae serologically since both have the same culture and biochemical characteristics

Hemophilus aegyptius clinical infection

conjunctivitis
can be epidemic levels in kids

Hemophilus aegyptius treatment

local administration of ophthalmis antibiotic solution

Chancroid

Hemophilus aegyptius clinical infection
venereal disease
initial infection causes formation of soft chancre (painful ulcerative sore on the genitalia that bleeds easily if scraped)
accounts for ~10% of all venereal diseases

Chancroid transmission

is by direct contact
is highly contagious

Hemophilus vaginale classification

was Gardnerella vaginalis for years until it was placefd in the Hemophilus genus because of DNA sequencing and hybridization results

Hemophilus vaginale clinical infection

venereal transmission that is associated with vaginitis
does not invade tissue but rather grows in vaginal secretions

Hemophilus vaginale identification

clue cells

clue cells

cquamous epithelial cells with adhered masses of Gram negative pleomorphic rods

Bordetella pertussis

causative agent of whoopign cough in humans
first isolated in 1906 by Bordet and Gengou
most commonly isolated Bordetella

Bordatella parapertussis

another pathogenic species of bordetella that causes similar illness as whooping cough

Bordetella pertussis laboratory diagnosis

gram negative rod
strict aerobe
requires selective enrichment media with 15-30% blood
slow grower: requires 2-5 days at 37°C to grow
current method of sample collections: collect nasopharyngeal sample on a dacron/rayon swab, assess for this using PCR or fluorescent antibody test
past method of sample collection: cough plate

Bordetella pertussis serological typing

contains species-specific capsular antigens: however, serological tests have not been sufficently standardized and approved for routine diagnostic use
lack of association between serum antibody levels and protective immunity makes results of serologic testing difficult to interpret

Bordetella pertussis source

usually children with the disease
healthy adults are reservoirs
major source: individuals with unrecognized milde pertussis such as those misdiagnosed with bronchitis, allergy, or walking pneumonia

Bordetella pertussis transmission

inhalation or direct contact with discharges from respiratory mucous membranes of infected persons
coughing aerosolizes bacteria thereby transmitting it to susceptible individuals

pertussis (whooping cough)

Bordetella pertussis clinical infection
following inhalation of infected droplets through nose or mouth
organism multiplis within the respiratory tract with an incubation period that varies from 5-21 days
after multiplication the organism aggregated on the bronchial and tracheal lining and toxins are releases
released exotoxin causes bacteria to adhere to cells, cytotoxicity and cell necrosis

Catarrhal

whooping cough stage
most highly infectious periods
lasts 7-14 days
upper respiratory involvement, mild cold-like symptoms
mild cough, sneezing, slight fever, runny nose

Paroxysmal

stage of whooping cough
lasts 1-6 weeks
cough during this stage is described as paroxysmal (sudden intensification of symptoms) or spasmodic (sudden but transitory airway constriction)
a series of coughs so close together and forceful that the person cannot take a breath between coughs
at the end of the cough spasm, the person gasps for breath which sounds like a whoop
coughing may be so intense and sever that vomiting follows the coughing episode
young infants usually do not whoop after coughing but may have anoxia, cyanosis, seizures, resultant encephalopathy

convalescence

stage of whooping cough
less evered and less frequent paroxysms

Bordetella pertussis complications

CNS disorders due to the anoxia have been associated with the disease (encephalopathy, coma after anoxic episode)
secondary infaction in the ears, sinuses, respiratory tract

Bordetella pertussis treatment

erythomycin is the drub of choice
susceptibility testing is not usually performed because of the characteristic slow growth of the organism
supportive treatment administered if needed
fluid and electrolyte management
oxygen therapy to avoid anoxia

Bordetella pertussis prevention

Vaccination is the primary method to prevent whooping cough, with DTaP or Tdap vaccines recommended.

DTap

vaccine given to children <7 years of age

TDap

booster immunization given at age 11 for continued protection

12 years

average duration og proective antibody titers following Bordetella pertussis vaccination

Brucella

in made up of bacteria that are intracellular parasites that infect lower animals and are transmissible to man

Brucella importance

causes contagious abortion in lower animals
causes brucellosis in humans
fever is undulant Irises and falls like a wave)

Brucella melitensis source

infected animals or secretions
animals mau recover quickly but excrete bacteria for varying lengths of time in secretions like milk

Brucella melitensis transmission

ingestion - contaminated milk or milk products
consumption - insufficiently cooked meat from infected animal
direct contact - at risk: dairymen, farmers, veterinarians
inhalation - rare but has occured in research lab workers

Brucella melitensis clinical infection

direct contact or ingestion
to initiate infection, bacteria
enter through the skin or are ingested
disseminate through lymphatics and blood stream
remain intact within phagocytes where they are protected from antibodies and from antibiotics
may cause abscess formation in infected tissue
localize in the spleen, bone maroow

Brucella melitensis symptoms

• nonspecific manifestations

  • weakness, fatigue usually manifested late in the day

  • chills, sweating

  • general malaise

  • anorexia, weight loss

  • abdominal pain, headache

• intermittent fever commonly called undulant fever

  • undulating characteristic is probably related to endotoxin release

• sometimes mental depression and increased nervousness

• symptoms last 3 months - 1 year normally but chromic may last up to several years with relapses

Brucella melitensis complications

arthritis, endocarditis, neurologic disorders

Brucella melitensis laboratory diagnosis

gram negative rod found intracellular in phagocytes, in tissue
slow growing bacteria: may take up to 30 days to grow
this organism is a biohazardous microbe at the BSL-3 level

Brucella melitensis other names

malta fever, Crimean fever, Gibraltar fever

Brucella melitensis treatment

frug of choise: tetracycline and or rifampin; alternative is chloramphenicol
antibiotics: intracellular localization of bacteria may contribute to antimicrobic ineffeciency or ineffectiveness

Brucella melitensis prevention

control animal infections (and meat from infected animal)
pasteurize milk and milk products

Franciella tularensis

gram negative rod found intracellular in macrophages
causative agent of tularemia
an acute infectious disease of wild animals, especially rabbits, ground squirrels

Franciella tularensis source

rabbits, rodents serve as reservoirs