Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
133 Cards in this Set
- Front
- Back
What are the pathogenic gram-negative cocci?
|
Neisseria mengitidis (AKA meningococcus)
Neisseria gonorrhoeae (AKA gonococcus) |
|
What do the Neisseria bacterium look like?
|
They are diplococci. Each coccus is shaped like a kidney bean, and a pair of cocci sticks together with their concave sides facing each other.
|
|
What does Neisseria mengitidis cause?
|
Meningitis
Life-threatening sepsis (meningococcemia) |
|
What are the virulence factors of Neisseria mengitidis?
|
1) Capsule: antiphagocytic
2) Endotoxin (LPS): causes blood vessel destruction (leading to petechial rash) and sepsis 3) IgA1 protease: cleaves IgA in half. |
|
What are the high risk groups for Neisseria mengitidis infection?
|
1) Infants aged 6 months to 2 years
2) Army recruits |
|
What are the symptoms of Meningococcemia?
|
The intravascular multiplication of Neisseria mengitidis results in abrupt onset of spiking fevers, chills, arthralgia (joint pains), and muscle pains, as well as petechial rash.
Can lead to meningitis and/or fulminant meningococcemia. |
|
What are the symptoms of fulminant meningococcemia?
|
AKA Waterhouse-Friderichsen syndrome. This is septic shock. Bilateral hemorrhage into the adrenal glands occurs, which causes adrenal insufficiency. Abrupt onset of hypotension and tachycardia, along with petechial skin lesions. DIC and coma may develop.
|
|
What are the symptoms of Neisseria mengitidis meningitis?
|
This is the most common form of meningococcal disease, usually striking infants <1 year of age. Symptoms include fever, vomiting, irritability, and/or lethargy.
|
|
How do you diagnose Neisseria mengitidis infection?
|
Gram stain and culture of the meningococcus from blood, CSF, or petechial scrapings.
Neisseria grow best on chocolate agar. The classic medium for culturing is called the Thayer-Martin VCN media (V for vancomycin, C for colistin, or polymyxin, and N for nystatin). Only Neisseria will be able to grow on this. |
|
What does Neisseria gonorrhoeae (AKA gonococcus) cause?
|
Neisseria gonorrhoeae cuases gonorrhea (the second most commonly transmitted sexual disease, after chlamydia)
|
|
What are the virulence factors of gonococcus?
|
1) Pili: The pili adhere to host cells. Complex genes coding for pili result in production of pili with hypervariable amino acid sequences. This protects the bacteria from our antibodies and vaccines.
2) Protein II: outer membrane protein is also involved in adherence to host cells. |
|
What is a structural difference between Neisseria gonorrhoeae and Neisseria meningitidis?
|
Meningococci contain a polysaccharide capsule and can ferment maltose. Gonococci do not have a polysaccharide capsule and cannot ferment maltose.
|
|
What are the symptoms of gonococcal disease in men?
|
Painful urination and purulent urethral discharge.
Complications of this infection include epididymitis, prostatitis, and urethral strictures. |
|
What are the symptoms of gonococcal disease in women?
|
Urethritis, with painful burning on urination, and purulent discharge from the urethra.
Pelvic inflammatory disease: infection of the uterus (endometritis), fallopian tubes (salpingitis), and/or ovaries (oophoritis). Patients present with fever, lower abdominal pain, abnormal menstrual bleeding, and cervical motion tenderness. |
|
What are complications of Pelvic inflammatory disease?
|
1) Sterility: most commonly caused by scarring of the fallopian tubes
2) Ectopic pregnancy 3) Abscesses 4) Peritonitis 5) Peri-hepatitis (Fitz-Hugh-Curtis syndrome) |
|
What is Peri-hepatitis?
|
AKA Fitz-Hugh-Curtis syndrome, this is an infection by Neisseria gonorrhoeae of the capsule that surrounds the liver. Patients complain of right upper quadrant pain and tenderness.
|
|
What are gonococcal diseases that can occur in both men and women
|
1) Gonococcal bacteremia
2) Septic arthritis |
|
What is ophthalmia neonatorum?
|
Ophthalmia neonatorum is a neonatal infection of the eye, due to transmission of Neisseria gonorrhoeae during delivery.
The infection can damage the cornea, causing blindness. This is prevented by giving all newborns erythromycin eye drops. |
|
What are the main groups of the enterics?
|
Enterobacteriaceae
Vibrionaceae Pseudomonoadaceae Bateroidaceae |
|
What are the three major surface antigens of the enterics?
|
1) O antigen: most external part of the LPS
2) K antigen: capsule that covers the O antigen 3) H antigen: subunits of the bacterial flagella |
|
What are the virulence factors of Escherichia coli?
|
1) Mucosal interaction:
a) Mucosal adherence with pili b) Ability to invade intestinal epithelial cells 2) Exotoxin production: a) Heat-labile and stable toxin (LT and ST) b) Shiga-like toxin 3) Endotoxin: Lipid A protion of LPS 4) Iron-binding siderophore: obtains iron from human transferrin or lactoferrin |
|
What are the diseases that Escherichia coli can cause?
|
Diarrhea
Urinary Tract Infection Neonatal Meningitis Gram-negative sepsis |
|
What are the three groups of diarrhea producing Escherichia coli?
|
1) Entertoxigenic Escherichia coli (ETEC)
2) Enterohemorrhagic Escherichia coli (EHEC) 3) Enteroinvasive Escherichia coli (EIEC) |
|
What is the presentation of Enterotoxigenic Escherichia coli (ETEC)?
|
This Escherichia coli causes traveler's diarrhea. It has pili (colonization factor) that help it bind to intestinal epithelial cells, where it releases toxins.
The toxins are heat labile toxin (LT) and heat stable toxin (ST). These exotoxins inhibit the reabsorption of Na+ and Cl- and stimulate the secretion of Cl- and HCO3- into the intestinal lumen, causing osmotic diarrhea. This stool looks like rice water - similar to cholera |
|
What is the presentation of Enterohemorrhagic Escherichia coli (EHEC)?
|
Bloody diarrhea, accompanied by severe abdominal cramps, called hemorrhagic colitis.
These Escherichia coli have pili, but also secrete Shiga-like toxin (verotoxin). This toxin inhibits protein synthesis by inhibiting the 60S ribosome, which causes intestinal epithelial death. |
|
What is hemolytic uremic syndrome (HUS)?
|
Hemolytic uremic syndrome (HUS) with anemia, thrombocytopenia, and renal failure is associated with infection by a strain of EHEC, called Escherichia coli 0157:H7.
Infections frequently seen in fast food chains. |
|
What is the presentation of Enteroinvasive Escherichia coli (EIEC)?
|
Immune-mediated inflammatory reaction with fever. Diarrhea is bloody with white blood cells. Similar to shigellosis.
|
|
What is the most common cause of urinary tract infection?
|
Escherichia coli
|
|
Which bacterium is encapsulated (with O antigen), but is nonmotile (no H antigen)?
|
Klebsiella pneumoniae
|
|
What does Klebsiella pneumoniae cause?
|
It is the second most common cause of sepsis
Urinary tract infections in hospitalized patients with Foley catheters Pneumonia: Alcoholics and hospitalized patients; bloody sputum (red currant jelly); abscess in lungs |
|
What is significant about Proteus mirabilis?
|
The organism is very motile, and is able to break down urea.
It is also a common cause of UTIs. Examination of the urine will reveal an alkaline pH, which is due to its ability to split urea into NH3 and CO2. |
|
What is the difference between Shigella species and Escherichia coli?
|
Shigella are nonmotile (have no flagella), does not ferment lactose, and does not produce H2S.
|
|
Is Shigella part of the normal intestinal flora?
|
It is never considered part of the intestinal flora.
|
|
What does Shigella cause?
|
Shigella invades intestinal epithelial cells and releases Shiga toxin, which causes cell destruction.
Symptoms are fever, abdominal pain, and diarrhea. Diarrhea may contain flecks of blood and pus (white cells). |
|
How does the Shiga toxin work?
|
There is an A subunit bound to 5 B subunits. The B subunits bind to the microvillus membrane in the colon, allowing for entry of the A subunit. The A subunits inactivate the 60S ribosome, inhibiting protein synthesis, causing cell death.
|
|
What is the difference between Salmonella and Shigella?
|
Salmonella is motile and produces H2S.
|
|
What is the Vi antigen?
|
Salmonella's Vi antigen is a polysaccharide capsule that surrounds the O antigen, thus protecting the bacteria from antibody attack on the O antigen.
|
|
What are the three common groups of Salmonella, and what are the respective diseases?
|
Salmonella typhi (Typhoid Fever)
Salmonella cholerae-suis (Sepsis) Salmonella enteritidis (Gastroenteritis) |
|
What is the pathogenesis and presentation of Salmonella typhi infection?
|
Salmonella typhi invades the intestinal epithelial cells, and invades the regional lymph nodes, finally seeding multiple organ systems. During this invasion, the bacteria are phagocytosed by monocytes and can survive intracellularly.
Typhoid fever: Fever Diarrhea Headache Rose spots on abdomen Abdominal pain (diffuse or localized to the right lower quadrant) |
|
Where do people recovering from typhoid fever harbor Salmonella typhi?
|
In the gallbladder
|
|
What population is particularly susceptible to Salmonella infections?
|
Salmonella is encapsulated with the Vi capsule. Patients who have lost their spleens have difficulty clearing encapsulated bacteria. Patients with sickle-cell anemia are particularly prone to Salmonella osteomyelitis.
|
|
What is the most common type of Salmonella infection?
|
Salmonella diarrhea, caused by any of hundreds of serotypes of Salmonella enteritidis.
|
|
How does Yersinia enterocolitica present? How is it transmitted?
|
Patients will develop fever, diarrhea, and abdominal pain (most severe in the right lower quadrant of the abdomen). It is transferred by the fecal-oral route following ingestion of contaminated foods, such as milk or fecally contaminated water.
|
|
What is the pathogenesis of Yersinia enterocolitica?
|
It possesses virulence factors that allow binding to the intestinal wall and systemic invasion into regional lymph nodes and the bloodstream.
This organism can secrete an enterotoxin, similar to that of E. coli, that causes diarrhea. |
|
What is different about Yersinia enterocolitica with regard to survivability?
|
Yersinia enterocolitica, unlike many types of bacterial pathogens, can survive and grow in the cold. It is not wiped out by refrigeration.
|
|
What bacteria causes cholera? How is it transmitted?
|
Vibrio cholera, transmitted via the fecal-oral route. Fecally contaminated water is usually the culprit.
|
|
What is the pathogenesis of Vibrio cholera?
|
Vibrio cholera attaches to the epithelial cells and releases the cholera toxin, choleragen. The disease presents with abrupt onset of watery diarrhea ("rice water" diarrhea) with loss of up to 1 liter of fluid per hour.
Cholera causes death by dehydration. |
|
What is Choleragen toxin similar to?
|
Choleragen has the same mechanism of E. coli's LT toxin (ETEC).
|
|
What organism causes gastroenteritis after ingestion of uncooked seafood (sushi), and is the leading cause of diarrhea in Japan?
|
Vibrio parahaemolyticus
|
|
What are the three most common causes of diarrhea in the world?
|
Campylobacter jejuni
ETEC Rotavirus |
|
How is Campylobacter jejuni transmitted?
|
It is a zoonotic disease, found in wild and domestic animals and in poultry.
Contaminated water (fecal-oral route) is often a mode of transmission. |
|
What is the illness of Campylobacter jejuni?
|
There is a prodrome of fever and headache, followed after half a day by abdominal cramps and a bloody, loose diarrhea. The organism invades the lining of the small intestine and spreads systemically.
|
|
What is the most common cause of duodenal ulcers and chronic gastritis?
|
Helicobacter pylori
(It is also the second leading cause of gastric ulcers, behind aspirin) |
|
How do you treat Helicobacter pylori infection?
|
Combinations of bismuth salts (Pepto-bismol), metronidazole, ampicillin, and/or tetracycline clears H. pylori and results in a decrease in both duodenal and gastric ulcer recurrence.
|
|
What are 8 important Pseudomonas aeruginosa infections?
|
1. Pneumonia
2. Osteomyelitis 3. Burn-wound infections 4. Sepsis 5. Urinary tract infections, pyelonephritis 6. Endocarditis 7. Malignant external otitis 8. Corneal infections |
|
What populations are susceptible to Pseudomonas aeruoginosa pneumonia?
|
Cystic fibrosis patients:most have colonies in their lungs. These patients develop chronic pneumonia, which progressively destroys their lungs.
Immunocompromised patients (cancer patients and ICU patients) |
|
What populations are susceptible to Pseudomonas aeruoginosa osteomyelitis?
|
Diabetic patients have an increased risk of developing foot ulcers infected with Pseudomonas aeruoginosa. The infection can penetrate into the bone resulting in osteomyelitis.
IV drug users have increased risk of osteomyelitis of the vertebrae or clavicle. Children develop osteomyelitis secondary to puncture wounds to the foot. |
|
What is significant about Bacteroides fragilis?
|
It is notable for being one of the few gram-negative bacteria that does not contain lipid A in its outer cell membrane (No endotoxin!). It does contain a capsule.
|
|
When does Bacteroides fragilis become pathologic?
|
When there is a tear in the intestine (bullet), surgery with bowel penetration, or when intestine ruptures secondary to infection (appendicitis) or ischemia. Bacteroides fragilis forms abscesses in the peritoneal cavity.
|
|
What confers the virulence of Haemophilus influenzae?
|
A polysaccharide capsule.
There are 6 types of capsules (a-f). Type b is commonly associated with invasive disease. |
|
Which capsule of the Haemophilus influenzae is the most invasive?
|
Type b is commonly associated with invasive Haemophilus influenzae disease in children, such as meningitis, epiglottitis, and septic arthritis.
|
|
How long does it take for children to develop their own antibodies against Haemophilus influenzae?
|
3-5 years
|
|
How do Haemophilus influenzae infections present?
|
Meningitis
Otitis media Acute epiglottitis Septic arthritis (Haemophilus influenzae is the most common cause in infants) Sepsis Pneumonia |
|
What is the drug of choice for serious H. influenzae infections?
|
A third generation cephalosporin, such as cefotaxime or ceftriaxone.
|
|
What are in the vaccinations for Haemophilus influenzae?
When are the vaccines given? |
Purified type b capsule (Hib) and diphtheria toxin (activates T-lymphocytes and antibodies against the b capsule).
Vaccines are administered at months 2, 4, 6, and 15. |
|
What species causes Chancroid? What is chancroid?
|
Haemophilus ducreyi is responsible for chancroid, which is a sexually transmitted disease.
It presents as a painful genital ulcer. Unilateral painful swollen inguinal lymph nodes rapidly develop in 50% of patients. Lymph nodes may rupture. |
|
How do you tell the difference between Haemophilus ducreyi chancroid and Syphilis ulcer?
|
Syphilis ulcers are painless, with painless, bilateral lymphadenopathy with no pus.
Chancroid ulcers are painful, with unilateral enlarged suppurative (pus-filled) lymph nodes. |
|
How do you tell the difference between Haemophilus ducreyi chancroid and Herpes?
|
Both herpes blisters (which can break) and chancroid ulcers are painful.
Herpes is usually accompanied by systemic systems such as myalgias and fevers. Chancroid does not produce systemic symptoms. |
|
What are clue cells? In which infections are they found in?
|
Clue cells are vaginal epithelial cells that contain tiny pleomorphic bacilli within the cytoplasm. They are found in Gardnerella vaginalis infections (vaginitis).
|
|
How do you treat Gardnerella vaginalis infections?
|
Metronidazole
|
|
How does the Bordetella pertussis toxin work?
|
Pertussis toxin has a B subunit that Binds to the target cell receptors, "unlocks" the cell, allowing entry of the A (Action) subunit. The A subunit activates cell-membrane bound G regulatory proteins, which in turn activate adenylate cyclase. This results in an outpouring of cAMP, which activates protein kinase and other intracellular messengers. This leads to 3 effects:
a) Histamine sensitization b) increase in insulin synthesis c) promotion of lymphocyte production and inhibition of phagocytosis |
|
What prevents the host defense from phagocytosing the Bordetella pertussis bacteria?
|
When attacking the bronchi, Bordetella pertussis throws out adenylate cyclase. The adenylate cyclase is swallowed by the host neutrophils, lymphocytes, and monocytes. The internalized adenylate cyclase then synthesizes the messenger cAMP, resulting in impaired chemotaxis and impaired generation of H2O2 and superoxide.
|
|
What function does the filamentous hemagglutinin (FHA) of the Bordetella pertussis bacteria have?
|
FHA is a pili rod extending from the surface of the bacteria that is involved in binding to ciliated epithelial cells.
|
|
What toxin of Bordetella pertussis is responsible of the violent cough?
|
Tracheal cytotoxin destroys the ciliated epithelial cells, resulting in impaired clearance of bacteria, mucus, and inflammatory exudate.
|
|
What are the stages of whooping cough?
|
1) Catarrhal stage
2) Paroxysmal stage 3) Convalescent stage |
|
In which stage of whooping cough is the disease most contagious?
|
Catarrhal stage: lasts from 1-2 weeks and is similar to an upper respiratory tract infection, with low-grade fevers, runny nose, sneezing, and mild cough.
|
|
What occurs during the paroxysmal stage of whooping cough?
|
The fever from the first stage subsides and the infected individual develops characteristic bursts of nonproductive cough. There may be 15-25 of these attacks per day, the attacks consisting of 5-20 forceful coughs followed by an inspiratory gasp through the narrowed glottis, which produces the characteristic whooping sound. During these paroxysms of coughing, the patient can become hypoxemic and cyanotic, the tongue may protrude, eyes bulge, and neck veins engorge. Vomiting often follows an attack.
This stage can last a month or longer. |
|
What would one see with the blood count of a patient with Bordetella pertussis whooping cough?
|
Examination of the white blood cell count will reveal an increase in the lymphocyte count with just a modest increase in the neutrophils (much like a viral infection).
|
|
Which aerobic gram-negative rod is ubiquitous in natural and manmade water environments?
|
Legionella pneumophila
|
|
How does Legionella pneumophila survive in the body?
|
Legionella pneumophila is a facultative intracellular parasite that settles in the lower respiratory tract and is gobbled up by macrophages. Once inside the macrophages, it inhibits phagosome-lysosome fusion, surviving and replicating intracellularly.
|
|
What is Pontiac fever?
|
Caused by Legionella pneumophila, the disease involves headache, muscle aches, and fatigue, followed by fever and chills.
Named after Pontiac, Michigan, where it struck 95% of the employees of the health department. |
|
What is Legionnaires' disease?
|
Patients develop very high fevers and a severe pneumonia.
|
|
How do you treat Legionella pneumophila infections?
|
Treat with erythromycin. It has a beta-lactamase making it resistant to penicillins. After treatment, find the source of the Legionella.
|
|
How do you diagnose Legionella?
|
It is gram-negative, but the organism is so small it will be hard to see on a gram stain. To see under the microscope, you must use silver stain.
You can grow the bacteria on charcoal yeast extract culture with iron and cysteine. |
|
What bacteria causes plague? How is it transmitted?
|
Yersinia pestis
Rats are the PESTS that harbor the disease, while fleas serve as the vectors, carrying Yersinia pestis to humans. During epidemics, the disease can also be seen as pneumonic plague with pneumonia and human-to-human transmission by aerosolized bacteria. |
|
What are the virulence factors of Yersinia pestis?
|
1) Fraction 1: Capuslar antigen that has antiphagocytic properties
2) V and W antigens: functions unknown |
|
What is the presentation of Yersinia pestis infection?
|
Swelling lymph nodes (usually inguinal), that become hot, red, and painful. Fever and headache set in, and hemorrhages under the skin cause a blackish discoloration ("Black death")
|
|
What bacteria causes a disease that is similar to bubonic plague, and is transmitted by handling infected rabbits and from bites of ticks and deerflies?
|
Francisella tularensis
|
|
What are the most important diseases found with Francisella tularensis?
|
1) Ulceroglandular tularemia: Following the bite of a tick or deerfly, or contact with a wild rabbit, a well-demarcated hole in the skin with a black base develops. Fever and systemic symptoms develop, and the local lymph nodes become swollen, red, and painful (sometimes draining pus). Bacteria can then spread to the blood and other organs. Similar to bubonic plague, but the skin ulcer is absent in plague, and mortality rate is only 5%.
2) Pneumonic tularemia: Aerosolization of bacteria during skinning and evisceration of an infected rabbit or hematogenous spread from the skin to the lungs can lead to a lung infection. |
|
Why will labs not culture Francisella tularensis?
|
Because the bacterium is so virulent (just 10 organisms can cause disease).
|
|
How do humans acquire Brucella?
|
From direct contact with infected animal meat or aborted placentas, or ingestion of infected milk products.
|
|
What is the pathogenesis of Brucella?
|
Brucella penetrates the skin, conjunctiva, lungs, or GI tract. This is followed by lymphatic spread, facultative intracellular growth in macrophages, and blood and organ invasion.
|
|
What are the symptoms of Brucella?
|
Systemic symptoms with fever, chills, sweats, loss of appetite, backache, headache, and sometimes lymphadenopathy. Fever usually peaks in the evening and slowly returns to normal by morning (undulant fever).
|
|
What bacterium causes the most frequent wound infection following a cat or dog bite?
What diseases are caused by this bacterium? |
Pastuerella multocida
Cellulitis and osteomyelitis |
|
What do you do with a patient who comes in with a cat or dog bite?
|
Do not close the wound with sutures. A closed wound creates a pleasant environment for Pasteurella multocida growth, and the resulting infection can invade local joints and bones.
|
|
What are two groups of gram-negative bacteria that are obligate intracellular parasites?
|
Chlamydia and Rickettsia
|
|
How do obligate intracellular bacteria survive?
|
Obligate intracellular organisms can only survive by establishing "residence" inside animal cells. They need their host's ATP as an energy source for their own cellular activity. They are energy parasites, using a cell membrane transport system that steals an ATP from the host cell and spits out an ADP.
|
|
What are some similarities and differences that Chlamydia and Rickettsia bacteria have with viruses?
|
Similar:
- Chlamydia and Rickettsia are very small. - They are obligatory intracellular parasites -They require animal cells to produce energy for them Different: - Chlamydia and Rickettsia contain both RNA and DNA, while viruses contain RNA or DNA, not both. - Chlamydia and Rickettsia are sensitive to antibiotics - They synthesize their own proteins |
|
What makes Chlamydia different from other gram-negative bacteria?
|
It does not have a peptidoglycan layer and has no muramic acid.
|
|
What is the life cycle of Chlamydia?
|
- The elementary body (EB) is a dense, round, small, infectious particle. The EB attaches to and enters (via endocytosis) columnar epithelial cells that line mucous membranes.
- Once within an endosome, the EB inhibits phagosome-lysosome fusion and is not destroyed. It transforms into an initial body (IB). - Once enough IBs have formed, some transform back into EB. - The life cycle is completed when the host cell liberates the elementary body, which can now infect more cells. |
|
What type of cells does Chlamydia like to invade?
|
Chlamydia is fond of columnar epithelial cells that line mucous membranes.
Thus, Chlamydia causes conjunctivitis, cervicitis, and pneumonia. |
|
What are the three species of Chlamydia, and what do they infect?
|
Chlamydia trachomatis: infects the eyes, genitals, and lungs
Chlamydia psittaci and Chlamydia pneumonia only infect the lungs. |
|
What is the leading cause of preventable blindness in the world?
What group is the most frequently infected? |
Trachoma, a type of chronic conjunctivitis. This is caused by Chlamydia trachomatis.
In the U.S., Native Americans are the group most frequently infected. |
|
What is the most common sexually transmitted disease in the U.S.?
|
Chlamydia trachomatis
|
|
What diseases can infect babies passing through the birth canal of a mother with chlamydia?
|
Inclusion conjunctivitis: Conjunctival inflammation with a purulent yellow discharge and swelling of the eyelids usually arises 5-14 days after birth. All newborns are given erythromycin eye drops prophylactically.
Infant Pneumonia: Usually occurs between 4-11 weeks. Initially, infant develops upper respiratory symptoms, followed by rapid breathing, cough, and respiratory distress. |
|
What are the symptoms of nongonococcal urethritis (NGU)?
|
Many patients are asymptomatic. Symptomatic patients develop painful urination (dysuria) along with a tin to thick, mycoid discharge from the urethra.
Caused by Chlamydia trachomatis |
|
What are the symptoms of cervicitis and pelvic inflammatory disease (PID)?
|
Cervicitis: Inflamed cervix appears red, swollen, and has yellow mucopurulent endocervical discharge. This infection can be caused by both Chlamydia trachomatis and Neisseria gonorrhoeae, and is called pelvic inflammatory disease (PID).
PID: abnormal vaginal discharge or uterine bleeding, pain with sexual intercourse (dyspareunia), nausea, vomiting, and fever. Most common symptom is lower abdominal pain. PID often results in fallopian tube scarring, which can cause infertility, tubal (ectopic) pregnancy, and chronic pelvic pain. |
|
What are the less common diseases caused by Chlamydia trachomatis?
|
Epididymitis
Reiter's syndrome: inflammatory arthritis of large joints Uveitis and conjunctivitis Urethritis Fitz-Hugh-Curtis syndrome: infection of the liver capsule with RUQ pain. |
|
What are the symptoms of Lymphogranuloma Venereum? What are the serotypes?
|
Symptoms: painless papule or ulceration on the genitals that heals spontaneously. Bacteria migrate to regional lymph nodes which enlarge over the next 2 months, and may become tender or break open.
Serotypes: Chlamydia trachomatis serotypes L1, L2, and L3. |
|
How do humans become infected with Chlamydia psittaci?
|
Chlamydia psittaci infects more than 130 species of birds, even pet parrots. Humans are infected by inhaling Chlamydia-lade dust from feathers or dried-out feces. Infection results in an atypical pneumonia called psittacosis.
|
|
What are the differences between Chlamydia and Rickettsia?
|
1) Rickettsia requires an arthropod vector (except Q fever)
2) Rickettsia replicates freely in the cytoplasm, while Chlamydia replicates in endosomes 3) Rickettsia has a tropism for endothelial cells that line blood vessels, Chlamydia likes columnar epithelium 4) Most Rickettsia cause rashes, high fevers, and bad headaches |
|
What bacteria shares antigenic characteristics with some Rickettsia?
What clinical implications does this have? |
Proteus vulgaris.
They strains that share these common antigens are designated OX-2, OX-19, and OX-K. The Weil-Felix reaction is a classic test that uses these cross-reacting Proteus vulgaris antigens to help confirm a diagnosis of a rickettsial infection. If a serum has antirickettsial antibodies, latex beads coated with Proteus antigens will agglutinate, indicating a positive Weil-Felix test. |
|
What causes Rickettsia rickettsii disease (Rocky Mountain Spotted Fever)?
What are the symptoms? |
Rocky Mountain Spotted Fever presents within a week after a person is bitten by either the wood tick (Dermacentor andersoni) or the dog tick (Dermacentor variabilis).
Disease is characterized by fever, conjunctival redness, severe headache, and a rash that initially appears on the wrists, ankles, soles and palms and later spreads to the trunk. |
|
What is the pathogenesis of Rocky Mountain Spotted Fever?
|
The organisms proliferate in the endothelial lining of small blood vessels and capillaries, causing small hemorrhages and thrombi. The inflammation and damage to small blood vessels explains the conjunctival redness and skin rash.
|
|
What disease does Rickettsia akari cause?
|
Rickettsial pox.
Rickettsia akari is carried by mites that live on house mice. |
|
What disease causes epidemic typhus?
|
Rickettsia prowazekii, carried by lice.
Symptoms: abrupt onset of fever and headache following a 2-week incubation period. Small pink macules appear around the fifth day on the upper trunk and quickly cover the entire body (But spares the palms, soles, and face). Patient may become delirious or stuporous. There is an increased risk of blood vessel clotting leading to gangrene of feet or hands. |
|
What disease causes endemic or murine typhus?
|
Rickettsia typhi, carried by fleas.
Symptoms: similar to epidemic typhus, but not as severe. Following a 10-day incubation period, fever, headache, and a flat and sometimes bumpy (maculopapular) rash develop. |
|
What organism causes trench fever (especially during WWI)?
|
Bartonella quintana, carried by lice.
|
|
What organism causes cat-scratch disease?
|
Bartonella henselae.
Symptoms: following a cat bite or scratch, regional lymph nodes will enlarge and the patient may develop low-grade fever and malaise. Disease usually resolves within a few months without complications. Bartonella henselae may also be responsible for bacillary angiomatosis, which involves proliferation of small blood vessels in the skin and organs in AIDS patients. |
|
What are the differences between Q fever and the other Rickettsiae?
|
Coxiella burnetii (Q fever) has an endospore form that gives the bacteria:
1) Resistance to heat and drying 2) Extracellular existence: allows survival outside a host cell 3) Non-arthropod transmission: Spores remain viable in dried tick feces deposited on cattle hides 4) Pneumonia: Spores inhaled into the lungs cause a mild pneumonia similar to that of Mycoplasma. |
|
What are the three genera of spirochetes?
What is unique about spirochetes? |
Borrelia, Leptospira, and Treponema
Mnemonic: BLT 1) They move in a unique spinning fashion via 6 thin endoflagella called axial filaments, which lie between the outer membrane and peptidoglycan layer and wrap around the length of the spirochete. 2) They replicate by transverse fission 3) They cannot be cultured in ordinary media, and are too small to be seen using light microscopy. |
|
Which bacterium causes syphilis? What is the pathogenesis of syphilis?
|
Treponema pallidum
Treponema pallidum enters the body by penetrating intact mucous membranes or by invading through epithelial abrasions. |
|
What are the three stages of syphilis?
|
Primary Syphilis: Painless chancre that erupts at the site of inoculation 3-6 weeks after initial contact. Regional nontender lymph node swelling occurs.
Secondary Syphilis: Bacteremic stage about 6 weeks after primary chancre has healed. Widespread rash, generalized lymphadenopathy, and involvement of many organs. Rash is small red macular (flat) lesions symmetrically distributed over the body, especially the palms, soles, and mucous membranes of the oral cavity. Condyloma latum: painless, wart-like lesion that occurs in warm, moist sites (vulva or scrotum), and is packed with spirochetes. Tertiary Syphilis: About 33% of patients progress to tertiary syphilis, which develops over 6-40 years. Results in: 1) Gummatous syphilis 2) Cardiovascular syphilis 3) Neurosyphilis |
|
What is Gummatous and Cardiovascular Syphilis?
|
Gummas are localized granulomatous lesions which eventually necrose and become fibrotic. These noninfectious lesions are found mainly in the skin and bones. Skin gummas are painless solitary lesions with sharp borders, while bone lesions are associated with deep gnawing pain.
Cardiovascular syphilis occurs at least 10 years after primary infection. An aneurysm forms in the ascending aorta or aortic arch, caused by chronic inflammatory destruction of small arterioles (vasa vasorum) supplying aorta. |
|
What are the five most common presentations in Neurosyphilis?
|
a) Asymptomatic neurosyphilis: clinically normal patient, but CSF tests positive for syphilis.
b) Subacute meningitis: fever, stiff neck, headache. CSF reveals high lymphocyte count, high protein, low glucose, positive syphilis. c) Meningovascular syphilis: spirochetes attack blood vessels in the brain and meninges, resulting in cerebrovascular occlusion and infarction of the nerve tissue in the brain, spinal cord, and meninges. d) Tabes dorsalis: affects the spinal cord, specifically the posterior column and dorsal roots. e) General paresis: progressive disease of the nerve cells in the brain, leading to mental deterioration and psychiatric symptoms. |
|
What is the rule of sixes for syphilis?
|
Rules of sixes:
Six-Sexual transmission 6 axial filaments 6 week incubation 6 weeks for the ulcer to heal 6 weeks after the ulcer heals, secondary syphilis develops 6 weeks for secondary syphilis to resolve 66% of latent stage patients have resolution (no tertiary syphilis) 6 years (at least) to develop tertiary syphilis |
|
What are the symptoms of congenital syphilis?
|
Early congenital syphilis: occurs within 2 years and is like severe adult secondary syphilis with widespread rash and condyloma latum. Snuffles (runny nose), lymph node, liver and spleen enlargement, and bone infection (osteitis) are also common.
Late congenital syphilis: similar to adult tertiary syphilis without cardiovascular involvement. Neurosyphilis and 8th nerve deafness is common. Bone and teeth involved. Saddle nose (inflammation destroys cartilage of palate and nasal septum), saber shins, Hutchinson's teeth, mulberry molars, and eye disease occurs. |
|
What is the Jarisch-Herxheimer Phenomenon?
|
Most patients with syphilis will develop an acute worsening of their symptoms immediately after antibiotics are started. Symptoms include a mild fever, chills, malaise, headache, and muscle aches. The killed organisms release a pyrogen.
|
|
What organism causes Lyme disease? What are the symptoms of early localized stage?
|
Borrelia burgdoferi, carried by the Ixodes tick.
Symptoms: The early localized stage begins 10 days after the bite and lasts 4 weeks. It consists of a skin lesion called erythema chronicum migrans along with flulike illness and regional lymphadenopathy. Erythema chronicum migrans (ECM) starts as a red flat round rash, which spreads out over time. The outer border remains bright red, while the center will clear, turn blue, or even necrose. |
|
What are the symptoms of early disseminated stage and late stage of Lyme disease?
|
The early disseminated stage involves the dissemination of Borrelia burgdorferi to four organ systems: skin, nervous system, heart, and joints.
Skin: multiple, smaller ECM lesions around the body Nervous: meningitis, cranial nerve palsies (Bells-CN VII), peripheral neuropathies. Cardiac: atrioventricular nodal block, myocarditis, left ventricular dysfunction. Joint: arthritis, muscle pain. Late stage: About 10% of untreated patients will develop chronic arthritis that lasts for more than a year. Can also cause chronic neurologic damage, leading to memory impairment, irritability, and somnolence. |
|
How are humans infected by Leptospira interrogans?
|
Leptospira are found in the urine of animals. These spirochetes can penetrate abraded skin or mucous membranes when humans come into contact with the urine either directly or by swimming in contaminated water (usually swallowed).
|
|
What are the two phases of leptospirosis?
|
First or leptospiremic phase: bacteria invade the blood and CSF, causing abrupt high spiking temperatures, headache, malaise, and severe muscle aches (thighs and lower back). Conjunctiva are red and patient has photophobia.
After about 1 week, there is a short afebrile period, and then the fever and earlier symptoms recur. This second or immune phase correlates with the appearance of IgM antibodies. During this second phase, patients may develop meningismus, and CSF reveals elevated white cell count. |
|
What is Weil's disease?
|
Leptospira interrogans can cause a severe illness called Weil's disease, or infectious jaundice, which involves renal failure, hepatitis with jaundice, mental status changes, and hemorrhage in many organs.
|