Unit 4 Exam
Chapter 18: Infectious Diseases of the Circulatory System
The Cardiovascular System
Composition and Functions of the cardiovascular system:
· Composed of blood vessels that carry blood to and from all regions of the blood, and the heart which pumps the blood. Provides tissues with oxygen and nutrients and carries away carbon dioxide and waste products.
Is the system closed or open? Closed
Defenses of the Cardiovascular and Lymphatic Systems
Cardiovascular system is highly protected from microbial infection:
- Microbes that successfully invade the system have access to every part of the body.
- Bloodstream infections are called systemic infections.
- List the defenses of the circulatory system. Leukocytes, lymphocytes, phagocytes.
Normal Biota of the Cardiovascular and Lymphatic Systems
- In a healthy state, what is the normal biota of the cardiovascular and lymphatic systems? Not completely sterile. Blood cells possibly contain bacteria.
- Recent studies from the HMP have suggested that the bloodstream is not completely sterile, even in periods of apparent health.
- These low-level microbial “infections” may contribute to diseases for which no etiology has been found or for conditions thought to be noninfectious.
COVID-19 Disease Table 18.1
- First pneumonia cases reported in Wuhan, China in Dec 2019
- The most acute and noticeable symptoms are in the respiratory system, but the virus can spread throughout the body via the cardiovascular system. This spread can cause varying degrees of damage for some time after the initial respiratory symptoms.
- Signs and Symptoms
o Range from none to death.
o Pneumonia, vomiting and diarrhea, skin rashes, muscle and joint, heart damage, blood clots.
o Virus is neurotropic- loss of taste, smell, headaches, long term cognitive decline, dementia.
o MIS-C
o Effects can be long-term (long Covid)
- Causative agents
o SARS-CoV-2
o Severe acute respiratory syndrome
o Alpha, Delta, Omicron, Arcturus
o Variants have individual transmissibility and virulence.
- Pathogenesis and virulence factors
o Viral S protein binds to host ACE-2 protein blocks its functions, dampens the inflammatory response. It leads to hyperinflammation.
o Immune complexes deposit in blood vessels: complement activation.
o Leads to the production of autoantibodies contributes to acute damage, worsening pre-existing autoimmune conditions, and also leading to new autoimmune conditions post-infection.
- Transmission and epidemiology
o Droplet and airborne (direct and indirect contact)
o The virus can infect some animals, mutate, and be transmitted back to humans.
- Prevention and treatment
o Face masks, social distancing
o mRNA vaccines, viral vector vaccine
o Vaccines are less effective at preventing cases but still protective against serious disease.
o Paxlovid, rebounding symptoms may occur.
Septicemia/Sepsis (organisms actively multiplying in the blood) Disease Table 18.2
Signs and Symptoms:
- Patients are very ill, have fever, and may have an altered mental state, shaking, chills, and gastrointestinal symptoms.
- Increased breathing rate
- Low blood pressure is the most dangerous feature of this condition:
o What causes the low bp? Inflammatory response to infectious agents in the bloodstream, which leads to a loss of fluid form the vasculature.
Causative Agents:
- Vast majorities are caused by which pathogen type? Bacteria
o Evenly divided between gram-positives and gram-negatives
- 10% are caused by fungal infections.
o Candida auris
- Polymicrobial bloodstream infections are being increasingly identified.
Pathogenesis and Virulence Factors:
- Gram-negative bacteria release large amounts of endotoxin.
- Gram-positive bacteria can instigate inflammation and a drop in BP when fragments of the cell wall are released into the blood.
Transmission and Epidemiology:
- It can often be traced to parenteral introduction.
- May arise from other sites of infection.
- Is the mortality rate high or low? high
Culture and Diagnosis:
- Blood culture
Prevention and Treatment: broad-spectrum antibiotics, then narrow-spectrum.
Endocarditis (inflammation of the endocardium, inner lining of the heart) Disease Table 18.3
Two variations of endocarditis, each with distinct groups of causative agents:
- Acute
- Subacute
Signs and Symptoms:
- Similar for both acute and subacute endocarditis
- Fever, fatigue, joint pain, edema, weakness, anemia, abnormal heartbeat, sometimes abdominal or side pain
- Patient may look very ill and have petechiae over the upper half of the body and under the fingernails.
- Janeway lesions: red, painless spots on palms and soles
- Osler’s nodes: small painful nodes on pads of fingers and toes
- Subacute cases:
o Enlarged spleen may have developed over time.
o Cases of extremely long duration can lead to clubbed fingers and toes due to lack of oxygen in the blood.
Acute endocarditis:
- Most often caused by Staphylococcus aureus
o “Vegetations” can form and hamper valve function. This can lead directly to cardiac malfunction and death.
o Pieces of bacterial vegetation can break off and create blockages in vital organs.
Transmission and Epidemiology of acute:
- Parenteral
o IV drugs
o Traumatic injuries and surgery
Subacute Endocarditis
- Almost always preceded by some form of damage to the heart valves or by congenital malformation.
- Causative Agents:
o Most commonly caused by bacteria of low pathogenicity, often normal biota from the oral cavity or skin
Transmission of subacute:
- Minor disruptions of skin or mucous membranes introduce bacteria into the bloodstream and lead to colonization:
o Rigorous tooth brushing or dental procedures
o Minor cuts and lacerations
Prevention:
- Antibiotics may be used in advance of surgical and dental procedures.
Treatment: broad-spectrum antibiotics, then narrow-spectrum for weeks
Cat Scratch Disease- Disease Table 18.5
Signs and Symptoms:
- Begin 1 – 2 weeks after infection.
- Starts with -cluster of small papules at the site of inoculation, lymph nodes may become enlarged and painful.
- What is the extent of most infections? Most infections remain localized and resolved on their own.
Causative Agent:
- Bartonella henslae: bacterium
- Transmitted among cats by fleas.
Transmission and Epidemiology:
- Transmitted by people by cat scratch or bite.
- 25,000 cases per year in the U.S.:
o 80% of cases are in children 2 – 14 years old.
Prevention and Treatment:
- Azithromycin, erythromycin, and rifampin can be effective.
- Avoid cat scratches/bites, use flea control, antiseptic cleaning of cat bite/scratch.
- Vaccine available? No
Spotted Fever Rickettsioses (Rocky Mountain Spotted Fever)- Disease Table 18.5
Causative agent:
- Rickettsia rickettsii, bacterium
Signs and Symptoms:
- After 2 – 4 days of incubation, symptoms are sustained fever, chills, headache, and muscular pain.
- Distinctive spotted rash occurs 2 – 4 days after the prodrome.
- Most serious manifestations are cardiovascular disruption.
- Convulsions, tremor, and coma can occur in untreated cases.
Transmission and Epidemiology:
- Hard ticks
Culture and Diagnosis:
- Isolation of rickettsias from the patient’s blood is best but difficult.
- DNA analysis can be performed on rash lesions.
Prevention and Treatment:
- Doxycycline
- Proper tick protection, long pants, DEET
Malaria- Disease Table 18.6
Signs and Symptoms:
10-day incubation period, first symptoms are:
- Malaise, fatigue, vague aches, and nausea with or without diarrhea, chills, fever, and sweating
- Symptoms occur at 48- or 72-hour intervals, as the result of synchronous rupture of what cell type? Red blood cells
Causative Agent: protozoa in the sporozoan group
Plasmodium species:
- List the five species that infect humans: P. malariae, P. vivax, P. knowlesi, P. ovale, and P. falciparum.
- Each shows variations in pattern and severity of disease.
o P. falciparum causes most deaths.
o P. vivax and P. ovale may be dormant in the liver up to 5 yrs.
Pathogenesis and Virulence Factors:
- Invasion of merozoites into RBCs leads to the release of fever-inducing chemicals into the bloodstream. Chills and fevers often occur in a cyclic pattern.
- Plasmodium also metabolizes glucose quickly, leading to hypoglycemia in the human host.
- Damage to RBCs results in anemia.
- Accumulation of malarial products in the liver and the immune stimulation in the spleen can lead to enlargement of these organs.
Transmission and Epidemiology:
- What is the transmission mechanism? Female anopheles’ mosquito
o What is geographical distribution? Restricted mostly to a belt extending around the equator.
o Are there any cases in the US? 2,000 new cases a year
Culture and Diagnosis:
- Discovery of Plasmodium in stained blood smears
Prevention:
- Vaccines are now available but are in low supply.
- Describe prevention for people living in endemic regions. Long-term mosquito abatement and human chemoprophylaxis. This includes elimination of standing water and spraying of insecticides. Also, netting, screens, and replants.
- Prophylactic drugs for travelers
- CRISPR techniques to make mosquitoes resistant to the parasite.
Treatment:
- Quinine and derivatives
o What are the drawbacks of these: toxicity, drug resistance, significant side effects?
- Artemisinin Combination Therapy
HIV Infection and AIDS- Disease Table 18.7
Causative Agent:
- HIV is an enveloped RNA retrovirus in the genus Lentivirus (Fig 18.13):
o Can only infect host cells that display a combination receptor consisting of the CD4 marker plus the coreceptor CCR-5.
o Contain reverse transcriptase (RT) What does this do? Catalyzes the replication of double-stranded DNA from single-stranded RNA.
o Retroviruses can permanently integrate viral genes into the host genome that is passed on to progeny cells. Some transform the host cells, making them malignant.
Signs and Symptoms:
- Symptoms of HIV are directly tied to two things (Table 18.2):
o The levels of virus in the blood
o The levels of T cells in the blood
- Initial symptoms:
o Fatigue, diarrhea, weight loss, and neurological changes
o Opportunistic infections or cancer
• AIDS-defining illnesses (ADIs): see table 18.3
- Other disease-related symptoms appear:
o Severe immune deregulation, hormone imbalances
o Pronounced wasting of body mass: consequence of weight loss, diarrhea, and poor nutrient absorption.
- Some of the most virulent complications are neurological:
o Lesions in the brain, meninges, spinal column, and peripheral nerves
o Withdrawal, persistent memory loss, spasticity, sensory loss, and progressive AIDS dementia.
Pathogenesis and Virulence Factors:
- Viral life cycle:
o HIV enters a mucous membrane or the skin and travels to dendritic cells beneath the epithelium. Virus grows inside the dendritic cell and is shed without killing the cell.
o The virus is amplified by macrophages in the skin, lymph organs, bone marrow, and blood. It infects and destroys helper T4 and CD4 lymphocytes, monocytes, macrophages, and B lymphocytes.
o The virus induces cell fusion, creating syncytia.
Transmission:
- HIV is mainly transmitted through:
o What are the 2 primary transmission mechanisms? Sexual intercourse and transfer of blood or blood products.
o Is virus transmitted through saliva, urine, tears, or sweat? No
o Babies can be infected before or during birth, or through breastfeeding.
Epidemiology:
- 35+ million have died worldwide since the epidemic began in the early 1980s.
- Estimated 40 million currently infected worldwide, 1.2 million in the US.
- Vertical transmission has declined.
Culture and Diagnosis:
- Most viral testing is based on detection of virus specific antibodies.
- In the U.S, diagnosis with AIDS requires:
(1) Testing positive for the virus and
(2) Meeting one of the following criteria:
• CD4 cells below 200 cells/microliter of blood
• Experience one or more AIDS-defining illnesses.
Prevention:
- Avoidance of sexual contact with infected people.
- Barrier protection (condoms)
- Avoid IV drugs.
- Preexposure prophylaxis (PrEP) is recommended to people at risk of infection.
Treatment:
- Is there a cure or vaccine protection? No
- Treatment guidelines are updated regularly.
o Many drugs are not widely available or are not affordable or practical.
- AIDS patients should receive a wide array of drugs to prevent or treat a variety of opportunistic infections and ADIs.
- A few people have cleared the virus after stem cell transplants.
Plague- Disease Table 18.8
Signs and Symptoms:
- Bubonic plague:
o Bacterium is injected by a flea bite, enters the lymph, and is filtered by a local lymph node.
o Infection causes inflammation and necrosis of the node, resulting in a swollen lesion called a bubo, usually in the groin or axilla.
o Chills fever; headache, nausea and weakness develop.
- Pneumonic plague:
o Respiratory disease, described in chapter 19.
- Septicemic plague:
o Presence of bacteria in the blood results in disseminated intravascular coagulation, subcutaneous hemorrhage, and purpura, which may degenerate into necrosis and gangrene.
o Because of the visible darkening of the skin, the plague has often been called Black Death.
Causative Agent:
- Yersinia pestis
o What type of pathogen is this? bacterium
Transmission:
- Mostly fleas
- Flea injects a blood meal from infected animal, bacteria multiply in its gut, causes coagulation and blockage of flea’s esophagus, ravenously jumps from animal to animal for nourishment, regurgitated infectious meal then is inoculated into bite wound.
Treatment and Prevention:
- Gentamicin, cipro, doxycycline
- Vaccine preventable? No not really
- Are there cases in the US? Who is most at risk? A few, sporadic cases. Vets and people living and working near woodlands and forests are most at risk.
Lyme Disease- Disease Table 18.10
Signs and Symptoms:
- Erythema migrans: lesion that looks like a bullseye. Is it a common sign? No, only about 10% of cases.
- List other early signs/symptoms. Fever, headache, stiff neck, dizziness.
- Can advance to the second stage:
o Cardiac and neurological symptoms
- Third stage:
o Crippling arthritis, severe neurological complications
Causative Agent:
- Borrelia burgdorferi: bacteria, spirochetes
Pathogenesis and Virulence Factors:
- The pathogen changes its surface antigens while it is in the tick and again after it has been transmitted to the mammalian host.
- It is possible that the immune response contributes to the pathology of the infection.
Transmission: hard ticks of genus Ixodes.
Culture and Diagnosis:
- Diagnosed early based on symptoms
- Tracking rising antibody titer
Prevention and Treatment:
- Protective clothing, boots, leggings, DEET, routine inspection
- Early, prolonged treatment with doxycycline or amoxicillin is effective.
Infectious Mononucleosis-Disease Table 18.8
Causative agent: Epstein-Barr virus
Signs and Symptoms:
- After a 30 – 50-day incubation period:
o Sore throat
o High fever
o Cervical lymphadenopathy
o Gray-white exudate in the throat
o Skin rash
o Enlarged spleen and liver.
o Leukocytosis
o Hallmark/most common symptom: fatigue
Transmission and Epidemiology:
- How common is this infection? Extremely
- Infection during the teen years seems to result in disease. Infections before or after this period are usually asymptomatic.
- Direct oral contact and contamination with saliva
Prevention and Treatment:
- No significant prevention
- Symptomatic relief
Chapter 19: Infectious Diseases Affecting the Respiratory System
The Respiratory Tract and Its Defenses
Divided into two parts
· Upper respiratory tract:
o Mouth
o Nose
o Nasal cavities and sinuses
o Throat/pharynx
o Epiglottis
o Larynx
· Lower respiratory tract:
o Trachea
o Bronchi
o Bronchioles
o Alveoli
Anatomical protection from infection:
· Nasal hairs
· Ciliary escalator
· Mucus
Second and third lines of defense
· Complement
· Antimicrobial peptides
· Macrophages
· Secretory IgA
Normal Biota of the Respiratory Tract
How does the composition of the upper respiratory tract differ from that of the lower? Thousands of normal biotas in upper respiratory tract vs. few normal biota
Some normal biota can cause serious diseases.
The composition of the lung microbiome differs in patients with COPD, asthma, and cystic fibrosis and between smokers and nonsmokers.
Name one benefit of the respiratory biota. Microbial antagonismà reducing the chance of a pathogen establishing itself.
Pharyngitis- Disease Table 19.1
Inflammation of the throat
Signs and Symptoms:
· Inflammation of the throat
· Swollen tonsils
· May also have
o Foul-smelling breath
o Difficulty speaking or swallowing.
o Headache
o May be white packets visible on the walls of the throat.
How do the signs/symptoms of viral pharyngitis compare to those caused by bacteria? Viral sore throats are mild and lead to hoarseness. Bacterial sore throats are painful and accompanied by fever, headache, and nausea.
Sore throats caused by bacteria are more painful than those caused by viruses, and more likely to be accompanied by fever, headache, and nausea.
Causative Agents:
· What types of viruses are common causes? Common cold viruses, strep pyogenes
· Name at least 2 non-infectious causes of pharyngitis: prolonged yelling, allergies, reflux
· Most serious cases of pharyngitis caused by Streptococcus pyogenes and Fusobacterium necrophorum.
Streptococcus pyogenes (Streptococcal pharyngitis)
· Type of pathogen? Gram morphology? Gram-positive, chains
Untreated streptococcal throat infections can result in serious complications.
o Scarlet fever: Sandpaper-like rash with high fever
o Rheumatic fever: due to an immunologic cross-reaction between streptococcal M proteins and the heart muscle
Transmission: respiratory droplets or direct contact with mucus secretions
Culture and Diagnosis (Remember Ex. 12 in lab?):
o Rapid diagnostic tests
o Culturing
Prevention: proper hand-washing
Treatment: penicillins, azithromycin
Fusobacterium necrophorum
· Gram morphology? Gram negative, bacillus
· Occurs commonly in adolescents and young adults.
· Can progress to Lemierre’s syndrome, leading to systemic infection.
· Usually, an endogenous infection that is treated with penicillin
The Common Cold- Disease Table 19.2
Causative Agent: Virus
· Rhinoviruses: 150 serotypes
· Coronavirus
· Adenovirus
· Respiratory syncytial virus
· Which is the most common? Rhinovirus
Transmission: Respiratory droplets
Symptoms:
· Sneezing
· Scratchy throat
· Runny nose
· Low fever in children
Prevention and Treatment: good hygiene and supportive treatment
Sinusitis (inflammatory condition of any of four pairs of sinuses in the skull) - Disease Table 19.3
Causative Agents:
· Various viruses or bacteria (often a mixed infection)
· Various fungi in immunocompromised patients
· Allergies and structural abnormalities are common noninfectious causes.
Treatment:
· When should antibiotics begin? After a week or so
· Broad-spectrum antibiotics for persistent bacterial infection
· Antifungals and/or surgery for fungal infection
Acute Otitis Media (fluid buildup and inflammation of middle ear and eustachian tubes) -Disease Table 19.4
The middle ear is sterile, so how do microbes get there? Migrate along the eustachian tube from upper respiratory tract.
Causative agents:
· The most common bacterial cause is Streptococcus pneumoniae.
· Candida auris
· Other bacteria/viruses
· Mixed biofilm of bacteria in chronic otitis media
Prevention: vaccines
· Prevnar
Treatment:
· What is “watchful waiting”? waiting 72 hours to allow the body to clear the infection
· When should antibiotics be used? Why shouldn’t antibiotics be administered as soon as signs and symptoms begin? In children with obvious drainage and rupture of tympanic membrane, antibiotics should be used. Many of the infections are caused by viruses that can clear up on their own.
· Tympanic membrane tubes
Pneumonia (inflammatory condition of the lung in which fluid fills the alveoli)
Pneumonia is an anatomical syndrome, the same set of signs/symptoms can be caused by a wide variety of different microorganisms (bacteria, fungi, viruses). Physicians often distinguish pneumonia into two forms, CAP and HCAP.
Community-Acquired Pneumonia- Disease Table 19.5
Streptococcus pneumoniae:
· Gram morphology? Gram-positive, flattened coccus
· Causes more lethal cases of pneumonia than any other microbe.
· Factors that favor the ability of the bacterium to cause disease:
o Old age
o Season
o Diabetes
o Underlying respiratory disease
· Treatment complications? Vaccine available? Immunization with PCV15 or PCV20
Legionella pneumophila:
· Gram morphology? Weakly, gram negative, dimorphic
· Water, amoebas, and ciliated protozoa
· Released during aerosol formation and carried long distances.
Atypical pneumonias:
· Mycoplasma and Chlamydophila
o Type(s) of pathogen? Bacterium
o Transmitted by aerosol droplets
“Walking pneumonia,” lacks acute illness.
Treatment consideration? Self-limiting, antibiotics if complications occur.
Histoplasma capsulatum (fungi):
· Highest incidence in eastern and central U.S.
· Where is the organism found in the environment? Moist soil, bird and bat droppings, chicken coops
Pneumocystis (carinii) jiroveci (fungi):
· Highly associated with which population subset? AIDs patients
· Likely transmitted through the inhalation of spores
· Traditional antifungal drugs are ineffective because of the chemical makeup of the cell wall.
Respiratory viruses:
· Very common causes of community-acquired pneumonia
o Either residents of the upper respiratory tract or acquired through daily activities, human metapneumovirus.
Is viral pneumonia generally more or less severe than bacterial and fungal pneumonia? Less severe
Treatment? Supportive only
Healthcare-Associated Pneumonia- Disease Table 19.6
Up to 1% of hospitalized or institutionalized people experience pneumonia. Most common form is VAP (what does that stand for? Ventilator-associated pneumonia
How does the mortality rate of HAP compare to CAP? What is the reason(s) for the difference? Mortality rate is usually much higher for HAP than CAP. HAP is often caused by MRSA and gram-negative bacteria. Polymicrobial.
Most frequent causes:
· MRSA
· Gram neg: Pseudomonas aeruginosa, Acinetobacter baumanii, Klebsiella pneumoniae, E. coli, Enterobacter (CRE)
· Many are polymicrobial in origin.
Transmission: Where do these pathogens usually come from? Microorganisms aspirated from upper respiratory tract
Culture and Diagnosis: Endotracheal tube or bronchoalveolar cultures provide useful information but are invasive.
Prevention and Treatment:
· Elevation of patients’ heads to a 45-degree angle helps reduce aspiration of secretions.
· Postoperative deep breathing and frequent coughing can reduce rates.
· Proper care of mechanical ventilators and respiratory therapy equipment
· Empiric therapy should begin as soon as hospital-associated pneumonia is suspected.
Influenza- Disease Table 19.7
Signs and Symptoms:
· Begin in upper respiratory tract.
· Can progress to lower tract.
· Headache, chills, dry cough, body aches, fever, stuffy nose, and sore throat.
Causative Agents: Influenza A, B and C
· Fig 19.8
Antigenic drift:
· Mutation of glycoprotein (H, N) genes
· Reduced host immune response to virus
· Produce seasonal outbreaks or pandemics? Seasonal outbreaks
Antigenic shift:
· RNA exchange between different viruses (Fig 19.10)
· Occurs during coinfection of a host cell.
· Produce seasonal outbreaks or pandemics? Pandemics
Pathogenesis and Virulence Factors
· Causes rapid shedding of ciliated cells of the respiratory mucosa.
· Cytokine storm
Transmission and Epidemiology:
· Inhalation of virus-laden aerosols and droplets
· Fomites
Culture and Diagnosis:
· Often diagnosed based on symptoms alone
· Culture and non-culture-based tests to identify virus subtypes.
Prevention: Vaccination
· Several types of influenza vaccine:
o Intramuscular, intradermal, nasal spray
· New vaccine prospects: Target epitopes shared by most flu viruses.
· Why are flu vaccines recommended every year? Dominant flu strains change every year.
· Can you get the flu from the flu vaccine? No
Treatment:
· Must be taken early in the infection.
· Zanamivir (Relenza)
o Inhaled drug
o Works against influenza A and B
· Oseltamivir (Tamiflu)
o Resistance does occur.
· Baloxavir (Xofluza)- newest
Whooping Cough (Pertussis)- Disease Table 19.8
Causative Agent: Bordetella pertussis: Bacteria
Transmission: respiratory droplets
Signs and Symptoms:
· Incubation phase: 3 – 21 days
· Catarrhal stage: characterized by runny nose, 1-2 weeks.
· Paroxysmal stage: bouts of severe coughing (paroxysm)
· Convalescent phase: no ongoing symptoms; susceptible to other respiratory infection
Prevention:
· Vaccine available? Dtap and Tdap
· Antibiotic treatment for contacts
· Why is pertussis returning to some populations? Fluctuations in vaccine rates
Respiratory Syncytial Virus- Disease Table 19.9
How common is this virus in the population? Very common
In what season(s) do cases peak? Winter and early spring
What age group is at risk for serious illness? Children 6 months or younger, premature babies, elderly
Transmission:
· Droplet and indirect contact via fomite
Virulence factor: “Giant cell” (syncytia) formation
Prevention:
· Passive antibody for high-risk children and babies under 8 months
· Vaccine available for adults over 60
Tuberculosis- Disease Table 19.10
Humans are easily infected with the bacterium but are resistant to the disease.
· Only 5-10% of infected people will develop a clinical case.
Primary Tuberculosis:
· High or low infectious dose? Low
· Bacteria multiply inside macrophages
· Escape leads to cell-mediated attack on bacteria.
· Tubercle formation in lungs
· Neutrophils release enzymes causing necrotic caseous lesions that heal by calcification.
Extrapulmonary Tuberculosis:
· Infection outside of the lungs:
o Lymph nodes, kidneys, bones, genital tract, brain, and meninges
· What groups are most at risk for this? Immunosuppressed patients and young children
Secondary (Reactivation) Tuberculosis:
· Pathogen is reactivated sometime after primary episode.
· Severe symptoms develop: “consumption.”
o Violent coughing, greenish or bloody sputum, low-grade fever, anorexia, weight loss, extreme fatigue, night sweats, and chest pain.
Causative Agent:
· Mycobacterium tuberculosis
· Bacteria
· Acid-fast rod
· Strict aerobe
· Neither gram neg or gram post.
· Grows very slowly.
Pathogenesis and Virulence Factors:
· How is the wall composition a virulence factor? Contains high content of complex lipids, including mycolic acid and waxes. It makes it resistant to drying and disinfectants.
· Stimulates strong cell-mediated immune response.
Transmission and Epidemiology: fine droplets of respiratory mucus suspended in the air.
Culture and Diagnosis:
· Clinical diagnosis of disease relies on these techniques:
o Tuberculin testing
o Blood testing
o Gene amplification and antibiotic susceptibility testing
o Acid-fast staining
Prevention:
· Patient isolation in negative-pressure rooms
· Vaccine used in the US. No How does vaccine alter/impact testing? May response positively to a TB skin test
Treatment:
· Depends on if infection is latent or active, 3-6 drugs given for 6-9 months.
· Why is noncompliance so common? Difficult to keep to a regimen of multiple antibiotics daily for months.
Drug-Resistant Tuberculosis
MDR-TB
Defined as being resistant to at least isoniazid and rifampin.
Requires treatment of 18 – 24 months with 4-6 drugs.
• XDR-TR
MDR-TB strains with resistance to two additional drugs
Few treatment options
Estimated 70% mortality rate within months of diagnosis.
Chapter 20: Infectious Diseases of the GI Tract
The Gastrointestinal Tract and Its Defenses
• Defenses against infection are extremely important:
– Mucus
– Secretory IgA found on most intestinal surfaces
– Muscular wall keeps things moving.
– Saliva à lysozyme
– Stomach acid
– Bile
Normal Biota of the GI Tract
• Normal biota of the oral cavity:
– Contains more than 600 known microbial species.
– Bacteria, fungi, and protozoa
• Stomach:
– 128 different species of microorganisms
• Normal biota of the large intestine:
– Harbors billions of microbes; 1011 per gram of contents
– Bacteria, fungi, protozoa, archaea
• Other functions of the normal biota:
– List at least 4 benefits/roles of the gut’s normal biota
• Development of nervous system
• Provides nutrients like vitamin K.
• Microbial antagonism
• Training the immune system
– Mix of microbiota in the gut can influence the host’s chances for obesity or autoimmune diseases.
• What is the normal biota of the accessory organs? None
Acute Diarrhea- Table 20.1
Diarrhea:
• How is “acute diarrhea” defined? Three or more loose stools in a 24hr period
• Often accompanied by fever, abdominal pain, cramping, nausea, vomiting, and dehydration
• In the U.S. acute diarrhea is transmitted by contaminated food.
• How are most cases of acute diarrhea treated? Replenishing fluids
1. Salmonella enterica
• Gram negative, rod
• About 10% of all chickens are infected
– Name at least 2 other common sources: rodents, reptiles
• Signs and Symptoms:
– Typhoid fever
• Common or rare in US? rare
– Salmonellosis (=enteric fever or gastroenteritis)
• Severe forms of salmonellosis can lead to septicemia.
– Milder forms of salmonellosis:
• Vomiting, diarrhea
• Mucosal irritation, Blood can appear in the stool.
• How long do symptoms usually last? 2-5 days
• Is Salmonellosis frequently fatal? No
• Pathogenesis and Virulence Factors:
– Ability to adhere to gut mucosa.
– Endotoxin
• Transmission and Epidemiology:
– High or low infectious dose? high
• Prevention and Treatment:
– Good hygiene, proper food handling
– How is uncomplicated salmonellosis treated? Fluid and electrolyte replacement
– Antibiotics used only in severe cases
2. Shigella
• Characteristics of Shigella:
– Gram negative, rod
– What is the reservoir? Humans
• Signs and Symptoms:
– Frequent, watery stools
– Fever
– Intense abdominal pain
– Nausea and vomiting are common.
– Dysentery: stools with blood and/or mucus
• Pathogenesis and Virulence Factors:
– Does Shigella perforate the intestine or invade the blood? No, enters intestinal mucosa by Peyer’s patches.
– Enters the large intestine mucosa and initiates inflammation.
– Endotoxin, enterotoxin, and Shiga toxin produced.
• Transmission and Epidemiology:
– How is it transmitted? Oral route, direct contact
• Large or small infectious dose? small
– Shigella can establish carrier conditions that can last months.
• Prevention and Treatment:
– Good hygiene
– How are uncomplicated cases treated? Supportive care
– Antibiotics may be used in immunocompromised patients.
3. Shiga-Toxin-Producing E. coli (STEC)
• Dozens of different strains of E. coli exist; most don’t cause disease.
• E. coli O157:H7 and its close relatives are the most virulent strains:
– What does STEC stand for? Shig-Toxin-Producing E. coli
• Signs and Symptoms:
– Mild gastroenteritis
– Fever
– Bloody diarrhea
– 10% of patients develop hemolytic uremic syndrome.
– Neurological symptoms such as blindness, seizure, and stroke
• Pathogenesis and Virulence Factors:
– Much of its virulence due to shiga toxins:
• What other bacterium produces shiga toxins? How did it get to E. Coli? Shiga toxins are genes present on prophage genes donated by bacteriophage in E. coli but are on the chromosome of Shigella dysenteriae.
• Interrupts protein synthesis on target cells and is responsible especially for systemic effects of the infection.
– Effaces enterocytes in the large intestine, resulting in bloody diarrhea.
• Transmission and Epidemiology:
– What is the most common mode of transmission? Ingestion of contaminated food
• Prevention and Treatment:
– Good food hygiene
– Are antibiotics used? No
– Supportive therapy, plasma transfusions
4. Campylobacter jejuni
• Gram negative, rod, with flagellum
• Probably the most common bacterial cause of diarrhea in the U.S.
– 2.4 million cases credited to it per year.
• Signs and Symptoms:
– Frequent, watery stools
– Fever
– Vomiting
– Headaches
– Severe abdominal pain
– How long do symptoms last? 2 weeks
• Pathogenesis and Virulence Factors:
– Transmission via ingestion of contaminated beverages and food:
• What are some common reservoirs? GI tract of poultry, domestic birds, livestock
– C. jejuni cells attach and burrow through the mucosa at the last segment of the intestine near its junction with the colon.
– Heat-labile enterotoxin stimulates secretory diarrhea.
– Guillain-Barré syndrome (GBS)
• 20 – 40% of GBS cases are preceded by an infection with Campylobacter.
– Treatment
• Rehydration and electrolyte balance
• Azithromycin treatment may be necessary.
• Antibiotic resistance is increasing in these bacteria. Why? Use of fluroquinolones in poultry industry
• Any vaccine protection? no Other preventative measures? Sanitary control of water and milk supplies, care in food preparation.
5. Clostridioides difficile
• Gram positive, rod, endospore former
• Causes pseudomembranous colitis (aka antibiotic-associated colitis)
• Signs and Symptoms:
– Diarrhea beginning late in antibiotic therapy or even after therapy has stopped:
• Severe cases exhibit abdominal cramps, fever, and leukocytosis.
• Colon is inflamed and gradually sloughs off loose, membranelike patches.
• Perforation of the cecum and death can result.
• Prevention and Treatment:
– Withdrawal of offending antibiotics and replacement therapy for lost fluids and electrolytes.
– Infections are treated with specific antibiotics until the intestinal biota returns to normal.
– Fecal transplants may be helpful.
– Hospitalized patients are isolated.
6. Vibrio cholerae
• Gram negative, rods, with single polar flagellum
• Signs and Symptoms:
– Vomiting followed by “rice water stools.”
– How can fluid loss impact overall health? Patients can lose up to 50% of body weight during disease, loss of blood volume, acidosis from bicarbonate loss, potassium depletion.
• Pathogenesis and Virulence Factors:
– High or low infectious dose? high
– Cholera toxin (CT):
• Shed large amounts of electrolytes into intestine, profuse water loss.
• Transmission and Epidemiology:
– Pattern of cholera transmission and the onset of epidemics are greatly influenced by the season of the year and the climate:
• Warm, monsoon, alkaline, and saline climates favor the migration of Vibrio.
– Bacteria survive in water sources for long periods of time.
– It can be spread by water and food.
• Prevention and Treatment:
– Proper sewage treatment and water purification
– Vaccine available? Yes, for travelers and people living in endemic regions.
– Oral rehydration therapy (ORT) should start early.
• Can restore patients in 4 hours.
– Antibiotics can shorten diarrhea and decrease bacterial excretion.
7. Rotavirus
• What is the global impact and prevalence of this virus? Primary viral causes of morbidity and mortality.
• Signs and Symptoms:
– Watery diarrhea
– Fever
– Vomiting
– Dehydration
– Shock
– Damage to the intestines can chronically compromise nutrition.
– Which group is at greatest risk of fatal disease? Babies from 6 to 24 months of age
– How is the disease different in adults? Mild and self-limiting
• Transmission: fecal-oral route, contaminated food, water, fomites
• Treatment:
– How are patients treated? Supportive care
– Vaccine available? No
8. Norovirus
• Second most common cause of hospitalizations from food-borne diseases in the U.S.
– Frequently affects the cruise ship industry.
• Transmission:
– Fecal-oral route, contaminated food, and water.
• Symptoms:
– Profuse, watery diarrhea for 3 – 5 days
– Vomiting and fever may accompany the disease.
• Treatment and prevention:
– Hygiene
– Vaccine available? No
– Rehydration
Food Poisoning- Disease Table 20.2
• Food poisoning should be suspected when:
– A patient presents severe nausea and frequent vomiting accompanied by diarrhea.
– Reports that companions with whom he or she shared a meal have the same symptoms.
• Symptoms in the gut that are caused by a preformed toxin:
– May be from microbial source or nonmicrobial source.
• Intoxication:
– Symptoms are severe after short incubation time.
1. Staphylococcus aureus Exotoxin
• Gram positive, cocci, clusters
• Associated with eating what type of foods: custards, sauces, cream pastries, processed meats, chicken salad, or ham that’s been left out for hours.
– Food has been contaminated by handling and left unrefrigerated.
– Will food containing the toxin look, smell, or taste different? No
– Exotoxin inactivation requires 100°C for at least 30 minutes.
• Ingested toxin acts on the gastrointestinal epithelium:
– Stimulates nerves causing symptoms of cramping, nausea, vomiting, and diarrhea.
• How quickly do patients recover? 24 hrs.
• Is the disease contagious or communicable? No
• What is the treatment? Supportive care
• What is the best prevention? Properly refrigerate food.
• Is this intoxication common or rare? Common
2. Bacillus cereus Exotoxin
• Gram morphology and cellular characteristics: sporulating, gram positive bacterium produces two exotoxins.
• What is the reservoir of these bacteria? Soil
• Emetic form:
– Linked to fried rice and pasta that has been cooked and kept warm for long periods of time.
• Diarrheal form:
– Usually associated with cooked meat or vegetables held at a warm temperature for long periods of time.
– Watery, profuse diarrhea that lasts for about 24 hours.
• Prevention: proper food handling
3. Clostridium perfringens Exotoxin
• Sporulating, gram positive bacterium
• Which types of foods are most commonly implicated? Animal flesh, vegetables
– When foods are cooled, endospores germinate and cells multiply, especially when food is not refrigerated.
• If the food is eaten without adequate reheating:
– Live C. perfringens cells enter the intestine and release exotoxin.
– Toxin acts on epithelial cells and initiates acute abdominal pain, diarrhea, and nausea in 8 – 16 hours.
• Prevention: thorough cooking food
Chronic Diarrhea- Table 20.3
• Diarrhea lasting longer than 14 days:
– Can have infectious or non-infectious causes.
• Irritable bowel syndrome and ulcerative colitis are noninfectious:
– Increasing evidence that a chronically disrupted intestinal biota can contribute to these conditions.
Giardia duodenalis (lamblia) (pathogenic, flagellated protozoan)
• Appearance: Symmetrical heart shape with 4 flagella
• Signs and Symptoms:
– Diarrhea of long duration
– Abdominal pain
– Flatulence
– Stools have a greasy and foul smell (hydrogen sulfide)
– Fever is usually not present.
• Transmission and Epidemiology:
– Often isolated from the intestines of animal and human carriers
– Cysts play a large role in transmission. How? Cysts can survive for 2 months in the environment.
• Prevention and Treatment:
– Human vaccine available? No
– Best prevention? Avoid drinking untreated water.
– Treatment with tinidazole or nitazoxanide
Dental Caries (Tooth Decay)- Table 20.4
• The most common infectious disease of people
• Symptoms range from:
– Minor disruption in the outer enamel surface of the tooth
– Complete destruction of enamel
– Destruction of deeper layers
• Deeper lesions can result in infection of the pulp, the location of the nerves. These lesions lead to toothache.
• Causative Agent:
– Streptococcus mutans
– How is it transmitted? Direct transfer
• Pathogenesis and Virulence Factors:
– In the presence of sucrose, S. mutans and other streptococci produce sticky polymers of glucose called fructans and glucans:
• These adhesives help bind them to the enamel surfaces and contribute to the bulk of the plaque.
– If plaque is not removed, it can result in a carious lesion:
• Streptococci and other bacteria produce acid as they ferment carbohydrates.
• Prevention and Treatment:
– Dietary restriction of sucrose and refined carbs.
– Regular brushing and flossing.
– Fluoride.
– Treatment of a carious lesion: removal of the affected part of the tooth and restoration with artificial material.
Periodontitis- Table 20.5
• Common or rare? Common
• Gingivitis:
– What are the most common signs/symptoms of gingivitis? Swelling, loss of normal contour, patches of redness, increased gum bleeding
• Periodontitis:
– Occurs if gingivitis is not treated.
– Increases the size of the pockets in the gum.
– It can cause bone resorption that can lead to tooth loss.
• Causative Agents:
– Caused by single species or polymicrobial infection? Polymicrobial infection
– If some of these enter the blood, other disease may result.
• Treatment:
– Removal of calculus and plaque
– Surgery to reduce the depth of periodontal pockets.
– Antibiotic therapy, either systemic or in periodontal packings, may be utilized.
Gastritis and Gastric Ulcers- Table 20.7
• Causative Agent:
– Helicobacter pylori: gram negative, rod, flagellum
• Signs and Symptoms:
– Gastritis: sharp or burning pain emanating from the abdomen.
– Gastric ulcers (aka peptic ulcers): lesions in the mucosa of the stomach or uppermost portion of the small intestine.
– Ulcers can be accompanied by bloody stools, vomiting, or both.
– Symptoms are often worse at night, after eating, or under conditions of psychological stress.
– Long term infection is linked to stomach cancer.
• Pathogenesis and Virulence Factors:
– Bacterium bores through the outermost mucus layer that lines the stomach epithelium and entrenches itself.
– Which enzyme does the bacterium use to persist in the highly acidic environment? Urease
• Transmission and Epidemiology:
– Reservoir unknown
– Transmission: oral-oral or oral-fecal route
– Long term infection linked to gastric adenocarcinoma cancer.
• Prevention and Treatment:
– Antibiotics augmented by acid suppressors
– Vaccine or other preventative measures? Diminish aggravating factors.
Hepatitis- Disease Table 20.8
• Inflammation and necrosis of the liver
– Patients may have jaundice: yellowish pigmentation of the skin, mucous membranes, sclera, deeper tissues, and excretions due to abnormal deposition of bile pigments.
• It can be caused by a variety of different viruses:
– We describe Hepatitis viruses A – E
• Noninfectious conditions that cause hepatitis:
– Autoimmune diseases
– Drug and alcohol abuse
1. Hepatitis A and E Viruses
• Both single-stranded, non-enveloped RNA viruses
• Both transmitted through the fecal-oral route.
• Both cause relatively minor, self-limited hepatitis.
• HEV can be a life-threatening infection in what groups? Pregnant people
• Signs and Symptoms:
– Subclinical or accompanied by vague, flu-like symptoms.
– Overt cases: Jaundice and/or swollen liver
– Are either HAV or HEV oncogenic? No
– In most cases, uncomplicated recovery results.
• Transmission and Epidemiology:
– Most infections result from:
• Unhygienic food handling
• Sexual transmission
• Travel to other countries.
– Hepatitis A can occasionally be spread by blood or blood products also.
– Does chronic infection occur with either infection? Hep E can rarely cause chronic infection in those with weak immune systems.
– Help A- humans.
– Hep E – humans and animals
• Prevention and Treatment:
– Prevention of hepatitis A is based primarily on immunization:
• Inactivated viral vaccine (Havrix) is available.
• Administration after exposure can prevent symptoms.
– Short-term protection can be conferred by passive immune globulin:
• Useful for people who have come into contact with HAV-infected people.
• Also used when people have eaten at a restaurant, which was the source of a recent outbreak.
– Vaccine available for Hep E? No
– Any specific treatment for either? Drinking fluids, avoiding alcohol and NSAIDs
2. Hepatitis B and D Viruses
• Hepatitis B virus (HBV):
– Enveloped DNA virus in the family Hepadnaviridae
• Hepatitis D virus:
– Enveloped RNA Virus
– Subvirus satellite of HBV:
• Can propagate only in the presence of HBV.
• Signs and Symptoms:
– Direct damage to liver cells:
• Fever, chills, malaise, anorexia, abdominal discomfort, diarrhea, and nausea
• Rashes may appear and arthritis may occur.
– HBV infection can be serious, even life-threatening:
• A small number of patients develop glomerulonephritis and arterial inflammation.
– Complete liver regeneration and restored function occur in most patients:
• A small number of patients develop cirrhosis or necrosis.
• Chronic HBV infection can lead to liver cancer.
• Transmission and Epidemiology:
– How is Hep B virus transmitted? Blood
• Even a minute amount of blood can transmit infection.
– Vertical transmission is possible:
• Predisposes the child to development of the carrier state and increases risk of liver cancer.
– Major infectious concern for healthcare workers
• HBV remains infective for days in dried blood, or months when stored in serum at room temperature, and for decades when frozen.
• Culture and Diagnosis:
– Serological tests can detect either virus antigen or antibodies.
• Prevention and Treatment:
– Vaccine available? Yes
– Passive protection with hepatitis B immune globulin (HBIG) gives immediate protection.
– How are mild cases of HBV are managed? Supportive care
– Chronic infection can be controlled with:
• Recombinant human interferon
• Antiviral drugs, are they curative? No
3. Hepatitis C Virus
• Sometimes called the “silent epidemic.”
• It takes many years to produce noticeable symptoms.
• Liver failure from hepatitis C is one of the most common reasons for liver transplants in the U.S.
• RNA virus in the family Flaviviridae
•
• Signs and Symptoms:
– People have widely varying experiences with this infection:
• 75 – 80% will remain infected indefinitely. Chronic infection can lead to hepatocellular carcinoma cancer.
– More common to have chronic liver disease even without overt symptoms.
– Worldwide, HBV infection is the most common cause of liver cancer. In the U.S., liver cancer is more likely caused by HCV.
• Transmission and Epidemiology:
– Blood and bodily fluids
• Prevention and Treatment:
– Vaccine available? No
– Treatment is tailored to which genotype of hep C virus is causing the infection, can be curative.
–
Gastrointestinal Tract Diseases Caused by Helminths
Pathogenesis and Virulence Factors in General
• The host’s response often damages the host body.
• Numerous adaptations to survive in their hosts:
– Specialized mouthparts for attaching to tissues and feeding.
– Enzymes with which they liquefy and penetrate tissues.
– Cuticle or covering to protect them from host defenses.
• Organ systems are reduced to the essentials:
– Getting food and processing it
– Moving
– Reproducing
Diagnosis follows a series of steps:
• O&P test
• A differential blood count showing eosinophilia.
• Serological tests indicating sensitivity to helminthic antigens.
• History of travel to or immigration from the tropics
• Discovery of eggs, larvae, or adults’ worms in stools or tissues
Prevention and Treatment in General
• Are vaccines available? No
• What are best prevention measures? Prophylactic treatment
• Why are many antihelmenthic drugs also toxic to humans? Helminths are eukaryotic, like human cells.
• In some cases, surgery may be necessary to remove worms or larvae.
1. Enterobius vermicularis
• Sometimes called the pinworm or seatworm:
– Common or rare? Common
– Most prevalent in which group? Children in temperate zones
• Transmission:
– Freshly deposited eggs have a sticky coating that causes them to lodge beneath the fingernails and onto fomites.
– Upon drying, eggs become airborne and settle in house dust.
– Eggs are ingested from contaminated food or drink, or self-inoculation.
– Eggs hatch in the small intestine and release larvae that migrate to the large intestine.
– There the larvae mature into adult worms and mate.
• Hallmark symptom: anal itching
• Other signs/symptoms? Disrupted sleep, nausea, abdominal discomfort, diarrhea.
• Scotch tape test can be used for diagnosis.
• When one member of the family is diagnosed, the entire family should be treated.
2. Cysticercosis- Table 20.11
• In pigs, Taenia solium eggs hatch in the small intestine:
– Released larvae migrate throughout the organs.
– Encyst in the muscles.
– Cysticeri: young tapeworms that are the infective stage for humans.
• When humans ingest live cysticerus in pork, the coat is digested and the organism is flushed into the intestine:
– What happens when the worm reaches human intestines? Firmly attaches by the scolex and develops into adult tapeworm.
• How is the course of infection different if humans ingest eggs? Eggs hatch in intestine and migrate to other tissues.
• One of the five neglected parasitic infections (NPIs) in the U.S.
• Neurocysticercosis:
– Larvae encyst in what location? brain
– Estimated that it is responsible for 10% of seizures in the ER in some US cities.
3. Schistosomiasis- Table 20.12
• Caused by the blood flukes Schistosoma
• Signs and Symptoms:
– Inflammation and swelling of spleen, bladder and liver may occur.
– Occasionally eggs are carried into the central nervous system and heart.
• Pathogenesis and Virulence Factors:
– How does the pathogen enter a human host? Burrow into unbroken human skin
– Coats itself with proteins from the host’s bloodstream
• Transmission and Epidemiology:
– Life cycle begins when humans release eggs into irrigated fields or ponds, either by deliberate fertilization with excreta or defecating or urinating in water.
– Life cycle is dependent on what type of intermediate host? Freshwater snails
– It affects 240 million people worldwide.
Chapter 21: Infectious Diseases of the Genitourinary Tract
The Genitourinary Tract and Its Defenses
Defenses of the urinary tract:
• Flushing action of the urine
Defenses in the urine itself: (List four)
1. acidic
2. lysozyme
3. lactoferrin
4. secretory IgA
Innate defenses of the male reproductive system:
• Flushing action of the urine
Innate defenses of the female reproductive tract (insert two):
1. Mucous membranes
2. Secretory IgA
3. Vaginal pH of about 4.5 during childbearing years
Normal Biota of the Genitourinary Tract
In both genders, the outer region of the urethra harbors some normal biota.
Principally known residents of the urethra:
• Nonhemolytic streptococci
• Staphylococci
• Corynebacteria
• Lactobacilli
How does the normal biota of the upper urinary tract compare to that of the lower? The lower urethra has a well-established microbiota, while the upper urinary tract appears to have fewer types and lower abundance.
Normal Biota of the Male Genital Tract
• Same as those listed for male urinary tract.
Normal Biota of the Female Genital Tract
• Vagina harbors normal biota.
• Lactobacillus species thrive.
• Candida albicans are also present at low levels.
• Same biota as urethra outside of childbearing years
How does the normal biota of the upper female reproductive tract differ than that of the lower? The upper female reproductive tract has occasional trespassers, and possibly permanent residents. The normal biota during childhood is the same as the urinary tract but varies as a female reaches childbearing years.
Urinary Tract Infections- Disease Table 21.1
Signs and Symptoms:
Cystitis is a disease of sudden onset:
• Frequent urges to urinate, even when the bladder is empty.
• Dysuria: burning pain with urination
• Pyuria: cloudy urine
• Hematuria: blood in urine
• Low-grade fever and nausea
Signs and symptoms of pyelonephritis (insert definition):
• Back/flank pain
• High fever
• What may happen if pyelonephritis if improperly or inadequately treated? Permanent kidney damage
Causative Agents:
• 95% of UTIs are caused by normal biota in the gastrointestinal tract:
– Of those, what bacterium is most commonly identified? E. coli
– Staphylococcus saprophyticus and Enterobacteriaceae are also common culprits.
Transmission and Epidemiology
• Are UTIs transmitted person to person? No
• Why are these more common in women than men? Nearness of urethral opening to the anus.
• Many women experience “recurrent urinary tract infections.”
– Some E. coli can invade the deeper tissue of the urinary tract and avoid being killed by antibiotics.
Treatment:
• Minimize use of urinary catheters to avoid infection.
• Sulfa drugs or nitrofurantoin are used for UTIs of various etiologies.
• Non-antibiotic drug phenazopyridine (Pyridium):
– What does this drug do? Relieve the burning and urgency symptoms.
– Why are some physicians reluctant to recommend it? It may mask worsening symptoms.
– Azo dye that turns the urine dark red or dark orange
• Why should penicillin drugs be avoided? Large percentage of E. coli strains are resistant to penicillin.
Reproductive Diseases Caused by Microorganisms
Are all reproductive tract diseases sexually transmitted? No
Vaginitis/vaginosis may or may not be sexually transmitted.
STIs are at an all-time high, after decades of progress.
• Discharge diseases are responsible for unprecedented numbers of infertility cases.
• Herpes and human papilloma virus (HPV) infections are incurable. What happens to their prevalence over time? They increase.
Gonorrhea- Disease Table 21.3
Causative Agent:
• Neisseria gonorrhoeae: pyogenic, gram-negative diplococcus
Signs and Symptoms:
• Male
– Urethritis
– Painful urination
– Yellowish discharge
– 10% of cases are asymptomatic.
– How can this lead to infertility? Scar tissue formed in the spermatic ducts.
• Female
– Mucopurulent (containing mucus and pus) or bloody vaginal discharge occurs in about half the cases (50% cases are asymptomatic).
– Painful urination if the urethra is affected.
– It can lead to salpingitis and/or pelvic inflammatory disease.
• Rare complications of gonococcal bacteremia are arthritis, rash, meningitis, and endocarditis.
• Children born to gonococcus carriers are in danger of being infected.
– Physicians screen pregnant mothers.
• Gonococcal keratitis can cause blindness. What preventative measure is taken with all newborn babies? Screening pregnant mothers for its presence and antibiotic eyedrops or ointments for newborns.
Pathogenesis and Virulence Factors:
• Fimbrial genes can rearrange themselves to put out fimbriae of different configurations:
– How does this help the pathogen? Confuses the body’s immune system. Antibodies that previously recognized fimbrial proteins may not recognize them once they are rearranged.
• IgA protease:
– What does this do? Cleave IgA molecules.
• Endotoxin
Transmission: sexual contact
Culture and Diagnosis:
• Antigen testing
• Males: gram stain of urethral discharge
Prevention: safe sex, condoms
Treatment: two antibiotics simultaneously
• Gonococcal Isolate Surveillance Project (GISP) run by CDC.
Chlamydia- Disease Table 21.3
C. trachomatis
• What type of pathogen? Bacterium
The most common reportable infectious disease in the US
• More than 1.5 million cases reported annually.
• Actual infection rate may be 5 – 7 times that number.
• At least 2 – 3 times as common as gonorrhea
Signs and Symptoms:
• 75% of cases are asymptomatic.
• Males:
– Discharge and painful urination.
– Untreated infections may lead to epididymitis.
• Females:
– Cervicitis
– Discharge
– Salpingitis
– PID
• What two types of infection are babies born to infected mothers most at risk for? Eye infections and pneumonia
Pathogenesis and Virulence Factors:
• Chlamydia is able to grow intracellularly:
– Unique cell walls prevent the phagosome from fusing with the lysosome inside phagocytes.
– The defensive inflammatory response leads to most of the actual tissue damage.
– Repair of inflammation leads to scarring, which can severely damage the fallopian tube.
Culture and Diagnosis:
• Usually determined by detection of antibody or antigen
• A urine test is available but is less accurate for females than males.
Prevention: safe sex, condoms
Treatment:
• CDC recommends annual screening of young women.
• Doxycycline or azithromycin
Vaginitis and Vaginosis- Disease Table 21.4
Signs and Symptoms:
• Vaginitis:
– Inflammation of the vagina
– Characterized by some degree of vaginal itching.
– Symptoms may include burning and discharge.
• Vaginosis:
– How is this different than vaginitis? Does not include significant inflammation.
Causative Agents:
• We will cover Candida, Gardnerella, and Trichomonas
1. Candida albicans: Vaginitis
• Characteristics:
– Dimorphic fungus
– Normal biota in 50 – 100% of humans. Name at least 2 other locations in or on the body where this resides. Mouth and GI tract.
• Vulvovaginal candidiasis:
– Presence of pseudohyphae in the smear of the vaginal secretions is a clear indication of the yeast growing rapidly and causing infection.
– Characterized by white, odorless, curd-like discharge and intense itching.
• Transmission and Epidemiology:
– Vaginal infections are nearly always opportunistic.
– Possible to transmit yeast through sexual contact:
– May act as normal biota in recipient.
• Prevention and Treatment:
– Vaccine available? No
– Topical and oral azole drugs are used to treat vaginal candidiasis, many available over the counter.
2. Gardnerella Species
• Vaginosis:
– Common condition in women in their childbearing years
– Doesn’t appear to induce inflammation in the vagina.
– Also known as bacterial vaginosis
– Mixed infection likely leads to disease.
– White to green, frothy discharge with fishy odor
• Pathogenesis and Virulence Factors:
– Mechanism of damage is not well understood.
– Can lead to PID, infertility, and ectopic pregnancies.
– Babies born to mothers with vaginosis have low birth weights.
• Transmission and Epidemiology:
– Is this a common rare disease in the US? Common
– Is this sexually transmitted? No, but it is common in sexually active females.
– Cause of bacterial overgrowth is unknown.
– Low pH typical of the vagina is higher in vaginosis.
• Culture and Diagnosis:
– What are “clue cells”? sloughed off vaginal epithelial cells nearly covered with adherent bacteria.
• Prevention and Treatment:
– Metronidazole or clindamycin
3. Trichomonas vaginalis
• Small, pear-shaded protozoa with four anterior flagella:
– It has no cyst form and does not survive long out of the host.
• Causes asymptomatic infections in approximately 50% of hosts:
• Are men frequently symptomatic or asymptomatic? Asymptomatic
• White to green, frothy discharge
• Complications of untreated infection: infertility, higher susceptibility to HIV
Genital Ulcer Diseases- Disease Table 21.6
Three common infectious conditions can result in lesions on the genitals:
• Syphilis
• Chancroid (we won’t cover)
• Genital herpes
Infection with an ulcer disease increases the chances of infection with HIV because of open lesions.
1. Syphilis
Causative Agent:
• Treponema pallidum: thin, gram-negative spirochete
• Marked by clinical stages designated as:
– Primary syphilis
– Secondary syphilis
– Tertiary syphilis
• Spirochete appears in the lesions and blood cultures during the primary and secondary stages, and is transmissible at these times:
– Also transmissible during the early latency period between secondary and tertiary syphilis
– Largely nontransmissible during the “late latent” and tertiary stages
Primary Syphilis
• Appearance of a chancre at the site of entry of the pathogen:
– Painless, hard
– Chancre heals spontaneously without scarring in 3 – 6 weeks.
– At this point, the spirochete has escaped into circulation and is entering a period of tremendous activity.
Secondary Syphilis
• Appears about 3 weeks to 6 months after the chancre heals:
– Many systems of the body have been invaded.
• Initial symptoms are:
– Fever
– Headache
– Sore throat
– Lymphadenopathy
– Peculiar red or brown rash that breaks out on all skin surfaces.
– Lesions contain viable spirochetes.
– Major complications linger for months and years.
Latency and Tertiary Syphilis
• 30% of infections enter a varied latent period that can last 20+ yrs:
– Antibodies to the bacterium are readily detected, but the bacterium is not.
– Is this common today? Why or why not? No, we have a widespread use of antibiotics.
– By the time a patient reaches this stage, numerous pathologic complications occur in susceptible tissues and organs.
• Cardiovascular syphilis:
– The aorta is subject to distention and fatal rupture.
– Aortic valves can also be damaged, resulting in insufficiency and heart failure.
• Neurosyphilis:
– It can involve any part of the nervous system.
– Diverse results include severe headaches, atrophy of the optic nerve, blindness, and dementia.
• Gummas:
– Nodular, infectious granuloma
Pathogenesis and Virulence Factors:
• Binds to the epithelium of mucus membranes by its hooked tip.
• Does the pathogen produce any toxin? No
• Although phagocytes act against it and antitreponemal antibodies are formed, immune responses are unable to contain it.
Transmission and Epidemiology:
· Rates have been increasing in the U.S. since 2003.
· This continues to be a serious problem worldwide, especially in Africa and Asia:
– People with syphilis often suffer from coinfections with other STIs, especially HIV.
Culture and Diagnosis:
· Detected rapidly by using dark-field microscopy of a suspected lesion.
· Blood tests based on antibody detection are used for diagnosis.
Prevention and Treatment:
· Best way to prevent transmission? Detection and treatment, safe sex
· Vaccine available? No
· Treat with antibiotics (ciprofloxacin, levofloxacin)
2. Genital Herpes
Causative Agent:
• Both HSV-1 and HSV-2 can cause genital herpes
Signs and Symptoms:
• Multiple presentations:
– After initial infection, a person may notice no symptoms.
– Could also cause the appearance of a single or multiple vesicles on the genitalia, perineum, thigh, and buttocks.
– Small, filled with clear fluid
– Are the vesicles painful? Yes
• Appearance of lesions may be accompanied by:
– Malaise
– Anorexia
– Fever
– Bilateral swelling and tenderness in the groin. What causes this? Inflammation of inguinal lymph nodes
• After initial recovery from infection:
– 4-5 recurrences
– Generally, less severe than the original symptoms
– Some people never have recurrent lesions.
– Encephalitis is a rare complication.
Pathogenesis and Virulence Factors:
• Herpesviruses have the tendency to become latent:
– Molecular basis of latency is not entirely clear.
– Name 2-3 stimuli that may trigger reactivation. Stress, UV radiation, injury, menstruation.
Transmission and Epidemiology:
• What is the primary route for transmission? Direct exposure to secretions
• Can genital herpes be spread when no lesions are present? Yes, constant shedding.
• Estimated that 20-40% of American adults are infected with HSV-2
Culture and Diagnosis:
• HSV-1 and HSV-2 can sometimes be diagnosed based on the characteristic lesions alone.
• Antibody and antigen to either virus can be detected from blood samples or lesions.
Prevention and Treatment:
• Vaccine available? No
• Best prevention? Safe sex, barrier protection methods
• Do antiviral cure infection? No, only reduce viral shedding.
Human Papillomavirus Infection- Disease Table 21.7
Causative Agent: human papillomaviruses
• Non-enveloped DNA viruses
• Over 100 different types of HPV
Signs and Symptoms:
• Warts:
– Outgrowths of tissue on the genitals, on anus, or skin around groin
• Appearance of warts:
– Tiny, flat, inconspicuous bumps
– Condyloma acuminata: extensively branching, cauliflower-like masses.
– Can be unsightly and obstructive.
• Certain types of viruses are oncogenic.
– What kind of cancers have been linked to HPV infection? Cervical, mouth, throat
Transmission and Epidemiology:
• How prevalent are HPV infections? Most prevalent STI
• Mode of transmission: direct contact
Treatment:
• Do antivirals or other treatments cure the infection? No
• Genital warts can be removed through a variety of methods.
• It is possible for the virus to resolve itself, but this is very unpredictable.
Prevention:
• Vaccination, safe sex
• Gardasil vaccine prevents infection from up to 9 types of HPV.
– Does vaccine fully prevent infection by any HPV strain? No
• Pap smear:
– Standardized screen for cervical cell changes
– Development can be stopped by removal of the affected tissue.