MVD is clinically indistinguishable from Ebola virus disease (EVD), and it can also easily be confused with many other diseases prevalent in Equatorial Africa, such as other viral hemorrhagic fevers, falciparum malaria, typhoid fever, shigellosis, rickettsial diseases such as typhus, cholera, gram-negative septicemia, borreliosis such as relapsing fever or EHEC enteritis. Other infectious diseases that ought to be included in the differential diagnosis include leptospirosis, scrub typhus, plague, Q fever, candidiasis, histoplasmosis, trypanosomiasis, visceral leishmaniasis, hemorrhagic smallpox, measles, and fulminant viral hepatitis. Non-infectious diseases that can be confused with MVD are acute promyelocytic leukemia, hemolytic uremic syndrome, snake envenomation, clotting factor deficiencies/platelet disorders, thrombotic thrombocytopenic purpura, hereditary hemorrhagic telangiectasia, Kawasaki disease, and even warfarin intoxication. The most important indicator that may lead to the suspicion of MVD at clinical examination is the medical history of the patient, in particular the travel and occupational history (which countries and caves were visited?) and the patient's exposure to wildlife (exposure to bats or bat excrements?). MVD can be confirmed by isolation of marburgviruses from or by detection of marburgvirus antigen or genomic or subgenomic RNAs in patient blood or serum samples during the acute phase of MVD. Marburgvirus isolation is usually performed by inoculation of grivet kidney epithelial Vero E6 or MA-104 cell cultures or by inoculation of human adrenal carcinoma SW-13 cells, all of which react to infection with characteristic cytopathic effects. Filovirions can easily be visualized and identified in cell culture by electron microscopy due to their unique filamentous shapes, but electron microscopy cannot differentiate the various filoviruses alone despite some overall length differences. Immunofluorescence assays are used to confirm marburgvirus presence in cell cultures. During an outbreak, virus isolation and electron microscopy are most often not feasible options. The most common diagnostic methods are therefore RT-PCR in conjunction with antigen-capture ELISA, which can be performed in field or mobile hospitals and laboratories. Indirect immunofluorescence assays (IFAs) are not used for diagnosis of MVD in the field anymore.

Since marburgviruses are not spreading via aerosol, the most straightforward prevention method during MVD outbreaks is to avoid direct (skin-to-skin) contact with patients, their excretions and body fluids, or possibly contaminated materials and utensils. Patients ought to be isolated but still have the right to be visited by family members. Medical staff should be trained and apply strict barrier nursing techniques (disposable face mask, gloves, goggles, and a gown at all times). Traditional burial rituals, especially those requiring embalming of bodies, ought to be discouraged or modified, ideally with the help of local traditional healers.

Marburg virus is a hemorrhagic fever virus of the "Filoviridae" family of viruses and a member of the species "Marburg marburgvirus", genus "Marburgvirus". Marburg virus (MARV) causes Marburg virus disease in humans and nonhuman primates, a form of viral hemorrhagic fever. Considered to be extremely dangerous, the WHO rates it as a Risk Group 4 Pathogen (requiring biosafety level 4-equivalent containment). In the United States, the NIH/National Institute of Allergy and Infectious Diseases ranks it as a Category A Priority Pathogen and the Centers for Disease Control and Prevention lists it as a Category A Bioterrorism Agent. It is also listed as a biological agent for export control by the Australia Group.

The virus can be transmitted by exposure to one species of fruit bats or it can be transmitted between people via body fluids through unprotected copulation and broken skin. The disease can cause bleeding (haemorrhage), fever and other symptoms much like Ebola. Funeral rituals are a particular risk. Actual treatment of the virus after infection is not possible but early, professional treatment of symptoms like dehydration considerably increase survival chances.

In 2009, expanded clinical trials of an Ebola and Marburg vaccine began in Kampala, Uganda.

Electron microscopy can reveal the bullet-shaped rhabdovirus, but is not

adequate for definitive diagnosis.

The Manual or Diagnostic for Aquatic Animals, 2006, is the standard

reference for definitive tests. In most cases, cell culturization

is recommended for surveillance, with antibody tests and reverse transcription

polymerase chain reaction (RT-PCR) and genetic sequencing and comparison

for definitive confirmation and genotype classification.

Virus neutralisation is another important method of diagnosis, especially for carrier fish.

Prevention of swine influenza has three components: prevention in pigs, prevention of transmission to humans, and prevention of its spread among humans.

The CDC recommends real-time PCR as the method of choice for diagnosing H1N1. The oral or nasal fluid collection and RNA virus preserving filter paper card is commercially available. This method allows a specific diagnosis of novel influenza (H1N1) as opposed to seasonal influenza. Near-patient point-of-care tests are in development.

The viral strains fall into two clades — Ravn virus and Marburg virus. The Marburg strains can be divided into two — A and B. The A strains were isolated from Uganda (five from 1967), Kenya (1980) and Angola (2004–2005) while the B strains were from the Democratic Republic of the Congo epidemic (1999–2000) and a group of Ugandan isolates isolated in 2007-2009.

The mean evolutionary rate of the whole genome was 3.3 × 10 substitutions/site/year (credibility interval 2.0–4.8).The Marburg strains had a mean root time of the most recent common ancestor of 177.9 years ago (95% highest posterior density 87–284) suggesting an origin in the mid 1800s. In contrast the Ravn strains origin dated back to a mean 33.8 years ago (early 1980s). The most probable location of the Marburg virus ancestor was Uganda whereas that of the RAVV ancestor was Kenya.

Thoroughly cleaning boats, trailers, nets and other equipment when traveling between different lakes and streams also

helps. The only EPA-approved disinfectant proven effective against VHS is Virkon AQUATIC (made by Dupont). Chlorine bleach kills the VHS virus, but in concentrations that are much too caustic for ordinary use. Disinfecting stations can be found at various inland lake boat launches in the Great Lakes region.

Spring viraemia of carp, also known as Swim Bladder Inflammation, is caused by a rhabdovirus called "Rhabdovirus carpio". It is listed as a notifiable disease under the World Organisation for Animal Health.

Clinical symptoms of viral infection include external hemorrhaging, pale gills, and ascites. In some cases, mortality can occur without any apparent clinical signs of the disease. The virus has been found in high concentrations in the liver and kidney, but lower numbers of virions have been isolated from the spleen. The virus has been shown to persist subclinically in fish populations up to 10 weeks following experimental infection. Currently efforts have been made to prevent infection by the virus through the development of DNA vaccines and immunostimulatory therapeutics.

This disease is diagnosed mainly by the appearance of well-demarcated rash and inflammation. Blood cultures are unreliable for diagnosis of the disease, but may be used to test for sepsis. Erysipelas must be differentiated from herpes zoster, angioedema, contact dermatitis, and diffuse inflammatory carcinoma of the breast.

Erysipelas can be distinguished from cellulitis by its raised advancing edges and sharp borders. Elevation of the antistreptolysin O titer occurs after around 10 days of illness.

The clinical symptoms are strikingly similar to those of lathyrism and also similar to tropical spastic paraparesis and hereditary spastic paraparesis, only that the latter two disorders have a slow onset. Konzo is distinct from polio which is a flaccid paralysis and most often affects a person asymmetrically.

A distinct myeloneuropathy also associated to cyanogen intake from cassava is tropical ataxic neuropathy (TAN), as first described in parts of Nigeria by B.O. Osuntokun in 1968. The disease is still occurring in the same areas.

The WHO has recommended three criteria for the diagnosis of konzo:

- a visible symmetric spastic abnormality of gait while walking or running;

- a history of onset of less than one week followed by a non-progressive course in a formerly healthy person;

- bilaterally exaggerated knee or ankle jerk reflexes without signs of disease of the spine.

Depending on its severity, konzo is divided into three categories: mild when individuals are able to walk without support, moderate when individuals need one or two sticks to walk, and severe when the affected person is unable to walk unsupported.

Crayfish plague, "Aphanomyces astaci", is a water mold that infects crayfish, most notably the European "Astacus" which dies within a few weeks of being infected. When experimentally tested, species from Australia, New Guinea and Japan were also found to be susceptible to the infection.

Depending on the severity, treatment involves either oral or intravenous antibiotics, using penicillins, clindamycin, or erythromycin. While illness symptoms resolve in a day or two, the skin may take weeks to return to normal.

Because of the risk of reinfection, prophylactic antibiotics are sometimes used after resolution of the initial condition. However, this approach does not always stop reinfection.

The diagnosis may be made on the clinical features alone, along with tests to rule out other possible causes. An EEG will usually show the electrical features of epilepsy and slowing of brain activity in the affected hemisphere, and MRI brain scans will show gradual shrinkage of the affected hemisphere with signs of inflammation or scarring.

Brain biopsy can provide very strong confirmation of the diagnosis, but this is not always necessary.

The diagnosis of group A beta-hemolytic streptococcus (GABHS) tonsillitis can be confirmed by culture of samples obtained by swabbing both tonsillar surfaces and the posterior pharyngeal wall and plating them on sheep blood agar medium. The isolation rate can be increased by incubating the cultures under anaerobic conditions and using selective growth media. A single throat culture has a sensitivity of 90–95% for the detection of GABHS (which means that GABHS is actually present 5–10% of the time culture suggests that it is absent). This small percentage of false-negative results are part of the characteristics of the tests used but are also possible if the patient has received antibiotics prior to testing. Identification requires 24 to 48 hours by culture but rapid screening tests (10–60 minutes), which have a sensitivity of 85–90%, are available. Older antigen tests detect the surface Lancefield group A carbohydrate. Newer tests identify GABHS serotypes using nucleic acid (DNA) probes or polymerase chain reaction. Bacterial culture may need to be performed in cases of a negative rapid streptococcal test.

True infection with GABHS, rather than colonization, is defined arbitrarily as the presence of >10 colonies of GABHS per blood agar plate. However, this method is difficult to implement because of the overlap between carriers and infected patients. An increase in antistreptolysin O (ASO) streptococcal antibody titer 3–6 weeks following the acute infection can provide retrospective evidence of GABHS infection and is considered definitive proof of GABHS infection.

Increased values of secreted phospholipase A2 and altered fatty acid metabolism in patients with tonsillitis may have diagnostic utility.

Embryos produced using in vitro fertilization may be genetically tested for HD using preimplantation genetic diagnosis (PGD). This technique, where one or two cells are extracted from a typically 4- to 8-cell embryo and then tested for the genetic abnormality, can then be used to ensure embryos affected with HD genes are not implanted, and therefore any offspring will not inherit the disease. Some forms of preimplantation genetic diagnosis—non-disclosure or exclusion testing—allow at-risk people to have HD-free offspring "without" revealing their own parental genotype, giving no information about whether they themselves are destined to develop HD. In exclusion testing, the embryos' DNA is compared with that of the parents and grandparents to avoid inheritance of the chromosomal region containing the HD gene from the affected grandparent. In non-disclosure testing, only disease-free embryos are replaced in the uterus while the parental genotype and hence parental risk for HD are never disclosed.

Crayfish plague first arrived in Europe in Italy in 1859, either with imported crayfish from North America, or in ballast water. After its original introduction in Italy in 1860, it spread quickly through Europe and was discovered in Sweden in 1907, in Spain in 1972, in Norway in 1971, in Great Britain in 1981, in Turkey in 1984 and in Ireland in 1987.

In 1959, to bolster dwindling stocks of native crayfish, the signal crayfish was introduced to Sweden. The signal crayfish was known to be resistant, and it was not recognised at that time that it was a carrier of the disease. After 150 years of contact, no resistance has been discovered in native European crayfish.

This species was studied and named by the German Mycologist, Friedrich Schikora (1859–1932), from a type specimen in Germany in 1906.

It is also possible to obtain a prenatal diagnosis for an embryo or fetus in the womb, using fetal genetic material acquired through chorionic villus sampling. An amniocentesis can be performed if the pregnancy is further along, within 14–18 weeks. This procedure looks at the amniotic fluid surrounding the baby for indicators of the HD mutation. This, too, can be paired with exclusion testing to avoid disclosure of parental genotype. Prenatal testing can be done when a parent has been diagnosed with HD, when they have had genetic testing showing the expansion of the HTT gene, or when they have a 50% chance of inheriting the disease. The parents can be counseled on their options, which include termination of pregnancy, and on the difficulties of a child with the identified gene.

In addition, in at-risk pregnancies due to an affected male partner, non-invasive prenatal diagnosis can be performed by analyzing cell-free fetal DNA in a blood sample taken from the mother (via venipuncture) between six and twelve weeks of pregnancy. It has no procedure-related risk of miscarriage (excepting via needle contamination).

It may be difficult to associate a particular case of diarrhea with a recent wilderness trip of a few days because incubation of the disease may outlast the trip. Studies of trips that are much longer than the average incubation period, e.g. a week for "Cryptosporidium" and "Giardia", are less susceptible to these errors since there is enough time for the diarrhea to occur during the trip. Other bacterial and viral agents have shorter incubation periods, although hepatitis may require weeks.

A suspected case of wilderness-acquired diarrhea may be assessed within the general context of intestinal complaints. During any given four-week period, as many as 7.2% of Americans may experience some form of infectious or non-infectious diarrhea. There are an estimated 99 million annual cases of intestinal infectious disease in the United States, most commonly from viruses, followed by bacteria and parasites, including Giardia and Cryptosporidium. There are an estimated 1.2 million U.S. cases of symptomatic giardiasis annually. However, only about 40% of cases are symptomatic.

One study suggests that on very long trips in the wilderness, taking multivitamins may reduce the incidence of diarrhea.

During the acute stage, treatment is aimed at reducing the inflammation. As in other inflammatory diseases, steroids may be used first of all, either as a short course of high-dose treatment, or in a lower dose for long-term treatment. Intravenous immunoglobulin is also effective both in the short term and in the long term, particularly in adults where it has been proposed as first-line treatment. Other similar treatments include plasmapheresis and tacrolimus, though there is less evidence for these. None of these treatments can prevent permanent disability from developing.

During the residual stage of the illness when there is no longer active inflammation, treatment is aimed at improving the remaining symptoms. Standard anti-epileptic drugs are usually ineffective in controlling seizures, and it may be necessary to surgically remove or disconnect the affected cerebral hemisphere, in an operation called hemispherectomy. This usually results in further weakness, hemianopsia and cognitive problems, but the other side of the brain may be able to take over some of the function, particularly in young children. The operation may not be advisable if the left hemisphere is affected, since this hemisphere contains most of the parts of the brain that control language. However, hemispherectomy is often very effective in reducing seizures.

Treatments to reduce the discomfort from tonsillitis include:

- pain and fever reducing medications such as paracetamol (acetaminophen) and ibuprofen

- warm salt water gargle, lozenges, or warm liquids

When tonsillitis is caused by a virus, the length of illness depends on which virus is involved. Usually, a complete recovery is made within one week; however, symptoms may last for up to two weeks.

The Tanganyika laughter epidemic of 1962 was an outbreak of mass hysteriaor mass psychogenic illness (MPI)rumored to have occurred in or near the village of Kashasha on the western coast of Lake Victoria in the modern nation of Tanzania (formerly Tanganyika) near the border of Uganda.