Published literature on S. putrefaciens, has reported sensitivity to aminoglycosides, fluoroquinolones, third/fourth-generation cephalosporins,

resistance to penicillin.

Pathogenicity studies of mice indicate that S. alga appears to be the more virulent species, possibly due to the production of a hemolytic substance.

In contrast, Shewanella putrefaciens organisms (Gilardi biovars 1 and 3; CDC biotype 1) were more often associated with nonhuman sources (70%)

certain virulence factors (hemolysis and adhesion).

Shewanella putrefaciens is as yet rarely responsible for clinical syndromes in humans

Nevertheless, S. putrefaciens also retains pathogenic potential, mainly under special environmental circumstances. Indeed, most of the reported infections pertained to contact with contaminated waters or injuries or occurrences in which integrity of the skin was compromised to some extent (3, 4, 9, 10, 12); this last issue encompasses also long-term catheters (1). In addition, isolation of S. putrefaciens occurred in polymicrobial infections (3).

Both S. putrefaciens and Shewanella alga are uncommon as isolates from clinical syndromes, their natural habitats being all forms of water, fish, oily foodstuffs, and soils (2, 4, 11)

Proteus and Enterobacter are only present in a minority of humans [64].

Ingestion of contaminated foods and direct contact

They are responsible for a variety of infections, including bacteremia, pneumonia, intravenous catheter-associated infections, osteomyelitis, endocarditis, and, rarely, endogenous and exogenous endophthalmitis

We report 16 cases of S. putrefaciens infection that occurred at the Veterans General Hospital-Kaohsiung in Taiwan between 1990 and 1995. S. putrefaciens infection was associated with a wide clinical spectrum including bacteremia/septicemia, skin and soft-tissue infection, biliary tract infection, peritonitis, and empyema.

Shewanella putrefaciens keratitis in the lamellar bed 6 years after LASIK.

Shewanella putrefaciens has only been isolated from such clinical materials as various body wounds, feces, conjunctiva, urine, CSF, bile, ascitic fluid, pleural fluid, and stored blood. The major risk factor of S. putrefaciens infection is hepatobiliary disease, peripheral vascular disease, with chronic leg ulcer, poor hygiene, and socioeconomic status. In most cases, the bacteria reside in devitalized tissue or denuded skin and serve as a nidus for opportunistic infection. Soft tissue infections have various clinical manifestations including infected leg ulcer, cellulitis, abscess formation, and wound infection, which are often preceded by chronic ulceration of the lower limb, trauma, burn wound, and seawater exposure.

β-lactamase antibiotics

treated easily by a combination of surgical therapy, drainage and antibiotics.

Thus we tried to find out as to how many of Shewanella spp. are wrongly reported as Pseudomonas spp. by just doing simple biochemical tests over a period of six months.

soil and water being their natural habitat

oxidase and catalase-positive non-fermenter gram-negative rod that produces hydrogen sulfide.

foods, sewage, and both from fresh and salt water.

Most Shewanella spp. isolates are susceptible to cefotaxime (95%), piperacillin and tazobactam (98%), gentamicin (99%), and ciprofloxacin (94%).

ear infection, or abdominal and biliary tract infections.

The patient was treated topically with moxifloxacin (0.5%) and tobramycin (15 mg/ml) drops every hour and cyclopentolate 2% three times daily in the right eye. N-acetylcysteine eye drops were administered four times per day.

Samples from conjunctival swabbing and corneal scraping, the contact lens, the cleaning solution, and the case were all submitted for microbiological analysis.

enterobac-teria (such asSerratia spp.andKlebsiella spp.) that can survive in contact lens fluid and onplastic surfaces, which explains their increased numbers incontact-lens-induced corneal infectio

CASE REPORTContact-lens-related corneal ulcer caused byklebsiella pneumoniae

hydrogen sulfide on TSI.[

On blood agar plates, the colonies are typically convex and large, with a brown pigment, and cause “greening” of the agar around the colonies.

bright pink color. On solid media, the colonies are round, fast-growing, and pink.

facultative anaerobe

marine environments

ENTEROBACTERIACEAE

multidrug-resistant Enterobacteriaceae (mostly Escherichia coli) that produce extended-spectrum β lactamases (ESBLs), such as the CTX-M enzymes, have emerged within the community setting as an important cause of UTIs.

Enterobacter spp. are commonly found in intensive care units and are responsible for 8.6 % of nosocomial infections according to the US Centers for Disease Control and Prevention

Positive. Immediately after the hydrogen peroxide solution had been added to a sample of the organism, it produced effervescence.

Negative. The sample on the cotton swab did not undergo a change in color several minutes after the reagent had been added.

Sorbitol – Positive. The organism is capable of fermenting sorbitol which results in the formation of acidic end products.

Lactose – Negative. The organism is not capable of fermenting lactose.

Indol formation – Negative. This indicates that the organism does not have the enzyme tryptophanase to metabolize tryptophan.

Glucose – Positive for the fermentation of glucose to produce acid, but negative for the production of gas.

Serratia marcescens was able to metabolize mannitol to produce acid, but gas was not produced.

Acid was produced causing a change in the color of the pH indicator to yellow, but no gas was produced. 

dark red colonies

bright, glossy red colonies on the TSA plate.

Results

Derivatives of prodigiosin have recently been found to have immunosuppressive properties and antitumor activity in vivo

capable of thriving in diverse environments, including water, soil, and the digestive tracts of various animals. [8] S marcescens has a predilection for growth on starchy foodstuffs, where the pigmented colonies are easily mistaken for drops of blood.

Some strains of S marcescens are capable of producing a pigment called prodigiosin, which ranges in color from dark red to pale pink,

Serratia are widespread in the environment, but are not a common component of the human fecal flora.

Mechanisms of Beta Lactam Resistance in Enterobacter

Glucose fermentation and acid production Lactose and/or sucrose fermenta-tion and acid production GYellow with bubbles or cracksGas production from glucos

38°C or below 36°C

a painful red eye

poor final visual outcome

urease-variable.[2][3]

RECOMMENDED MEDIA

16-18 hours.

KEY BIOCHEMICAL REACTIONS

Facultatively anaerobic

20-30 degrees C

Spores: No.

are susceptible to cefepime(7), aminoglycosides, fluoroquinolones, and trimethoprim-sulfamethoxazole(8). Tigecycline has been shown effective in vitro

Gram-negative bacilli, 0.6-1 μm in diameter and 1.2-3 μm long, motile by means of peritrichous flagella and have class 1 fimbriae

Enterobacter spp. are resistant to ampicillin; first- and second- generation cephalosporins(7); and cephalothin

Person to person transmission can occur through the fecal-oral route

Enterobacter spp. are commonly found in soil and water;

Structure

d negative-sense, single-strand RNA virus. This means that the virus has genetic material that consists of a single strand of RNA that has the opposite sequence to messenger RNA. Therefore, the genetic information must be converted by RNA polymerase in order to be translated into a protein and carry out its function. There are two major glycoproteins on the surface of RSV and they are called the attachment glycoprotein (G) and the fusion glycoprotein (F) (3). These proteins with sugar attached to them can be found in or around the membrane of cells, and ultimately play an important role in the initial phases of the infection (3).

Mastomys natalensis

e Lassa virus

Mild symptoms include slight fever, general discomfort or illness, weakness and headache. However, the other 20% of infected individuals experience more serious symptoms such as hemorrhaging in gums, eyes or nose, respiratory issues, nausea and vomiting, swelling in the face, pain in check back or abdomen and even shock. There have also been incidences of neurological problems including hearing loss, tremors, and brain swelling. In these cases, death may occur within two weeks of the first showing symptoms due to multi-organ failure [3

animal borne

the first to die from the disease.

Vs) detected worldwide, July 2009 - March 2011 (29)

There have been no serious side effects caused by IPV which is why there has been a pushed to change to vaccine method in order to reduce VDPV and eventually eradicate the disease.

y Sabin wild type strains. Most commonly by wild type 3 and 2.

at can grow in the gut of

attenuated

positive stain of Poliovirus

reduced the polio cases.

pe 1 and 3 are currently foun

paralysis.

quire their envelope

psids bud into the ER lumen.

These polyproteins are cleaved by viral proteases to form a smaller proteins that form the viral replicase and allow the virus to synthesize a negative sense template and subgenomic postive sense RNAs. The negative sense template is used to produce the positive sense viral genome that will be encorporated in to new viruses, while the subgenomic RNAs encode all viral proteins.

While research into the

tory drugs are the only treatment, since no

re severe respiratory problems

There are also rarer symptoms including gastrointestinal symptoms such as diarrhea, which is important considering other coronaviruses cause gastrointestinal diseases

The disease is caused by new virus of the family coronaviruses (Groneberg, 2005). Viruses of this family are spherical, have an envelope, contain RNA which can be directly translated inside the host (positive sense RNA). Their surface is also covered in "spikes" of glyoproteins, which produce the "corona" effect under an electron microscope which gives them their name (Groneberg, 2005). The SARS coronavirus (SARS-CoV) genome was sequenced in 2003 and was distinct from any other coronavirus found in humans or human-associated animals (Groneberg, 2005).

viral respiratory disease

Summary:

Congenital infection, however has much worse prognosis and a higher mortality rate (approximately 35%).

Symptoms of LCM tend to present itself within 8 to 13 days after contracting the virus. There are various phases in which the infection presents itself as disease. The initial phase of the disease includes symptoms such as fever, malaise, lack of appetite, muscle aches, headache, nausea, and vomiting. After recovery from the initial phase, a second phase of illness may occur. Symptoms that coincide with the second phase of illness include meningitis (inflammation of the meninges), encephalitis (drowsiness, confusion, sensory disturbances), and meningoencephalitis (inflammation of the brain and the meninges).

help them fight off infection

The Lymphocytic Choriomeningitis Virus (LCMV)

The spread of smallpox has decreased dramatically.

A biopsy or x-ray can be performed to examine whether the patient is showing signs of a viral infection.

f symptoms that are general enough

creates a localized pus-filled rash.

making it highly contagious.

s variola.

of smallpox i

careful treatment of current patients with the disease, they made it possible.

family and functions as effectively as cowpox.

vaccinia

vaccinated. T

effective process for smallpox was confirmed,

ollowing with smallpox r

o get vaccinated out of fear.

Edward Jenner played a key role in developing a vaccine for smallpox. Prior to his research, dried pus-filled scab material would be scratched onto a person's skin to expose the uninfected person to the disease.

vaccination for smallpox decreased significantly in the early 1980s.

h high mortality and contagious levels, fi

incredibly

onomic and sanitary conditions

r

Some common symptoms of EBV include: fatigue, inflammation of the throat and lymph nodes, fever, rash, swollen liver, and enlarged spleen (2).

As stated earlier, humans are the primary reservoir for EBV. Though there is a great deal that is not clearly understood about the entry mechanisms used by EBV, there have been experiments done in vitro that provide the most probable mechanisms (1). In order for a successful entry into a B cell, an interaction between EBV glycoprotein called gp350 and a protein complement receptor called CR2/CD21 is needed (1). Once the virus binds to this respective site, it is endocytosed into a low pH compartment (1). This low pH environment helps initiate the fusion of the "core fusion machinery", which is a common mechanism of virus-cell fusion among all herpesviruses (4). This core fusion machinery contains four glycoproteins that help mediate fusion B-cell fusion (4). It is hopeful that future research will reveal these entry mechanisms of the EBV virus so a vaccine can be developed to provide immunity.

virus is approximately 122-180 nm in diameter and is a double-stranded helix of DNA which contains about 172,000 base pairs and 85 genes (5). The DNA is surrounded by a protein shell called a nucleocapsid which is surrounded by clusters of protein called a tegument (5). This tegument then is surrounded by an envelope of lipids and surface projections of glycoproteins that are integral in the infection of the host cell (5).

s usually accompanied by a recovery period of two to four weeks i

EBV causes infectious mononucleosis (mono) a

viral

HPIV can be efficiently removed from surfaces with most common detergents, disinfectants, or antiseptic agents.1

zoonotic

s children and the elderly.2 Other groups likely to show symptoms are those suffering from malnutrition, vitamin A deficiency, babies not being breastfed, and those exposed to environmental toxins such as smoke

-2 is less detecte

causing lower respiratory diseases.

36% of all reported cases r

. Other rare cases a human can contract the virus is if an infected mice bites someone, or touch or eat anything that came into contact with infected mice droppings, urine, or saliva (CDC).

lation of aerosolized mouse droppings.

ot spread from person to person.

o several Native American Tribes.

four corners

Hantavirus Cardiopulmonary Syndrome (HCPS), is mostly common in the western states. 96% of reported cases of HCPS have occurred in states west of the Mississippi River.

ude fever, headache, muscle aches, and chills, and progresses to a severe respiratory disease that can eventually lead to death

the deer mouse was the primary carrier of the virus

re was an outbreak in the southw

rdiopulmonary Syndrome in humans

Human adenoviruses lack a viral envelope composed of proteins and lipids that surround the viral capsid (1). They are generally 65nm to 80nm in diameter, and are composed of a protein capsid and a nucleoprotein core that contains the viral genome (double-stranded DNA, 26-46 kbp, containing 23-46 protein coding genes) (1). Depending on the viral subgroup, the human adenovirus has a range of diversity (1). Within subgroups (A, B type 1, B type 2, C, D, E, F, G), the human adenovirus serotypes share between 48% and 99% of their DNA; between subgroups, however, there is less than 20% shared (1).

AdV antibodies in their bodies, i

Human adenoviruses cause a number of diseases, most often conjunctivitis, gastroenteritis, hepatitis, myocarditis, and pneumonia

85 deaths per year in the United States caused by the disease. In recent years, however, this number has shrunk to about 8.

The vaccines are not 100% effective, but in cases where vaccinated children do still contract the disease, it is half as contagious as it is when the virus infects unvaccinated children

VZV does not have to be transmitted via direct contact, although contact with secretions from a person infected with VZV can result in infection. One of the primary ways that VZV is transmitted is through respiratory pathways.

specific place

enpox (which typically occurs in children), and shingles. Shingles can occur in adults who had chickenpox as children when the virus, which remained latent in the Dorsal Root Ganglia, becomes active again.

Dorsal Root Ganglia until it is reactivated later in life and becomes Shingles.

t most are familiar with.

ng the mucosa,

x and can reoccur later in adults as Shingles.

Vector

fter a large surge in infections in 2012.

euroinvasive diseases like encephalitis,

94% of cases

be transmitted through blood transfusions or organ transplants.

mosquito-bird-mosquito cycle

virus can be food- or water-borne, and it can survive on physical surfaces, which can lead to viral outbreaks in environments such as schools or cruise ships.2

Several laboratory tests, such as enzyme-linked immunosorbent assay (ELISA), can diagnose CCHFV by detecting specific molecules (antigens) or RNA sequences unique to the virus [

with mortality rates of up to 30% [1

e 1: Lytic Cycle of a Virus

HSV-1 and HSV-2 can also go into periods of latency, meaning the virus is not actively being produced in the host (Nicoll, Proenca & Efstathiou, 2012). During latency, the host is absent of disease and no transmittance can occur (Nicoll, Proenca & Efstathiou, 2012). The host acts as a reservoir during latency and periodically the virus reactivates and the host can infect others (Nicoll, Proenca & Efstathiou, 2012). There are currently no vaccinations or prophylactic measures to completely prevent the spread of herpes (Akhtar & Shukla, 2009). The use of condoms and washing ones hands are effective methods to prevent the spread of herpes (“Herpes Simplex Virus”).

HSV-1 and 2 binds to receptors on epithelial cells triggering the fusion with the cell (Karasneh & Shukla, 2011). Once inside the cell, viral DNA enters the nucleus and allows for viral transcription through the lytic cylce (Nicoll, Proenca & Efstathiou, 2012). The lytic cycle is the process in which viruses overtake cells and uses host machinery to reproduce and results in the killing of the host cell to release the virus to infect surrounding tissues (Figure 1)

Genital and oral herpes is transmitted through skin-to-skin contact and mucous membrane contact with an infected individual (Nicoll, Proenca & Efstathiou, 2012). Herpes can be transmitted through sexual intercourse and kissing

capsid and are surrounded in a lipid bilayer

ffects as inflammation in the brain, blood disorders, eye infections, deafness, and others

the CSF is produced (2). The virus then replicates within these areas and can penetrate into the brain and destroy some of the epithelial integrity, causing it to disintegrate into the CSF (2).

re, leading to meningitis and encephalitis (

s, bleeding, fluid build-up, and the death of local exocrine and skin cells

such as sports teams and classrooms

though research of the development and spread of the virus are primarily done through animal studies (2). MuV belongs to the family Paramyxoviridae. The virus is enclosed in a protein shell (2) and seven linked transcription units (2). It is infect healthy cells by fusing its membrane to the membrane of a target cell (2), and these infected cells are able to attach to other healthy cells to spread the infection (2).

While mumps is a disease t

Regular contact with infected individuals such as hugging, kissing, sharing drinks and utensils, and shaking hands does not transmit the disease.

riends of those infected (WHO, 2016).

sever. T

Disease Prevalence and Demographic

Figure 1: The path of HIV through the host cell. Source: Becerra et al. (2016)

Once inside the body, the virus uses the host's cells by "hijacking the cell’s machinery" and replicating its own genomic material along with the DNA of the host (Becerra et al., 454).

Proteins DNM1/Dynamin 1 or DNM2/Dyamin 2 function to pinch the plasma membrane to enclose the virus in a Clathrin Coated Vesicle (CCV), and bring the CHIKV virus into the cytoplasm (Viralzone).

ith mechanisms similar to that of other alphaviruses, with selectivity for receptors not found on all types of cells (Solignat et. al). CHIKV has demonstrated selectivity for proliferation in various cell types such as microphages, the kidney epithelial cell line (HEK-293T), the hepatocarcinoma epithelial line (HUH7), lung cells (MRC-5), skeletal muscle cells, and various endothelial cell lines (ThRBMEC and hCMEC/D3) (Solignat et. al).

as binding to receptors, on the host cell membrane (

he host cell and

Two structural proteins encoded by the CHIKV RNA strand, E1 and E2

arboviruses

skyrocketed

veremic

The Chikungunya virus itself is a type of Alphavirus (Weaver et. al, 1231), which are structurally characterized by having eighty trimeric glycoprotein spikes (1) which allow the virus entry into the host cell (Snyder and Mukhopadhyay) via promoting the fusion of viral and target host cell membranes (Yang et. al).

Coxsackievirus contains various dips along it's virion surface in which the binding occurs. By doing so, instability occurs allows for a fatty acid to be released.

Once attached to the receptor, the virus binds to it

external

Marburg haemorrhagic fever

Risk factors

Transmission route for 183 (52%) was foodborne, 74 (21%) unknown, 50 (14%) person-to-person, 31 (9%) waterborne, 11 (3%) animal contact, and 1 (0.3%) laboratory-related

The incubation period can range from 3 to 8 days

Treatment in severe cases is electrolyte replacement (to provide electrolytes, such as sodium, potassium and chloride ions, lost through vomiting and diarrhoea) and rehydration.

The most common symptoms of Salmonella Enteritidis include fever, diarrhea, vomiting, abdominal cramps, muscle aches, and headache. These symptoms generally occur between 12-72 hours after the bacteria has been ingested and last anywhere from 4-7 days. Healthy individuals can usually rid themselves of the bacteria on their own; however, children, elderly people, and those with compromised immune systems may require additional treatment [18].

Once established in the intestine, the bacteria's virulence factors go to work. An enterotoxin results in the release of fluids from the cell into the lumen. This factor is responsible for the diarrhea and vomiting symptoms. Next, the endotoxin results in the release of endogenous pyrogens from the host cell, causing a fever in the victim. Lastly, the cytotoxin is responsible for the disintegration of the cytoplasm.

TABLE 1. Number of cases and incidence of confirmed infections,* hospitalizations, and deaths, by pathogen — Foodborne Diseases Active Surveillance Network, United States, 2015†

monella spp. (-) (99)

Salmonella enterica ATCC® 14028 A 24hr 35°C Aerobic Growth; colorless to amber colonies

Salmonella enterica ATCC® 14028 A 24hr 35°C Aerobic Growth; colonies colorless