Metastasis to spermatic cord from carcinoma prostate: A case series

Despite the high incidence of secondaries to lymph nodes, bones, and lungs in carcinoma (CA) prostate, metastatic involvement of scrotal organs is rare and usually associated with a poor prognosis. Here, we report a case series of three cases of CA prostate with metastatic involvement of scrotal organs. All three patients had metastatic involvement of the spermatic cord, with involvement of epididymis in the first patient and testes in the third patient, revealed incidentally on orchiectomy. Two patients were also found to have coexisting lymphatic filariasis. To date as per the best of our knowledge, only one such case of CA prostate with metastasis to scrotal organs and associated filariasis has been reported. This highlights the need for histopathological evaluation of all orchiectomy specimens. Chronic infection and inflammation leading to lymphatic obstruction due to filariasis probably led to the unusual retrograde spread of the tumor.

Retrograde Spread of Buccal Space Infection into Temporal Space with Temporal Muscle Necrosis in a Medically Compromised Patient - A Case Report

Superficial temporal space lies between the temporal fasciae. Abscess in the temporal and infratemporal space is very rare. They develop as a result of the extraction of infected maxillary molars. Temporal space infections or abscesses can be seen in the superficial or deep temporal regions. A 65 - year - old male patient reported with a complaint of painful swelling over the right cheek and restricted mouth opening with a history of extraction of second mandibular molar before four weeks. On examination, an ill-defined diffuse swelling was seen. Treatment was started with IV empirical antibiotics and planned for surgical drainage. Surgical drainage of the abscess in the temporal space was done along with debridement of the necrosed temporalis muscle. Infections of the maxillofacial region are of great significance to general dentists and maxillofacial surgeons. They are of clinical importance as they are commonly encountered, and are also challenging as timely intervention is needed to prevent fatal complications. The infections arising from the tooth are initially confined to the alveolar bone and surrounding periosteum. They spread along the path of the least resistance to the cortical plates. Once the infection penetrates the cortical plates, they reach the muscle plane.1 If the infection perforated is above the muscle attachments, it’s confined to an intraoral abscess. If the cortical plates are perforated below the muscular attachments, extraoral swelling develops. The next barrier is the periosteum which is strong and elastic in nature. Once the periosteum is breached, infections reach the soft tissue planes, the fascia. Most of the infections are confined to a particular space and the surrounding fascia. Based on the toxins produced by the microorganisms, the infection can spread to adjacent spaces and even retrograde. Common deep space infections are Ludwig's angina followed by peritonsillar, submandibular, and parotid abscesses. 2 Infratemporal and temporal space infections are rarely compared to other deep space infections. Many etiological factors form the base for the infections of deep spaces, dental caries, extraction of infected, non-infected tooth maxillary sinusitis, tonsillitis, maxillary sinus fracture, temporomandibular arthroscopy, drug-induced infections. Infections of odontogenic origin, spreading along infratemporal and temporal space are most common with maxillary molars followed by mandibular molars. We report a case of retrograde spread of buccal space infection into temporal space secondary to mandibular tooth extraction.

Retrograde Spread of Buccal Space Infection into Temporal Space with Temporal Muscle Necrosis in a Medically Compromised Patient - A Case Report

Superficial temporal space lies between the temporal fasciae. Abscess in the temporal and infratemporal space is very rare. They develop as a result of the extraction of infected maxillary molars. Temporal space infections or abscesses can be seen in the superficial or deep temporal regions. A 65 - year - old male patient reported with a complaint of painful swelling over the right cheek and restricted mouth opening with a history of extraction of second mandibular molar before four weeks. On examination, an ill-defined diffuse swelling was seen. Treatment was started with IV empirical antibiotics and planned for surgical drainage. Surgical drainage of the abscess in the temporal space was done along with debridement of the necrosed temporalis muscle. Infections of the maxillofacial region are of great significance to general dentists and maxillofacial surgeons. They are of clinical importance as they are commonly encountered, and are also challenging as timely intervention is needed to prevent fatal complications. The infections arising from the tooth are initially confined to the alveolar bone and surrounding periosteum. They spread along the path of the least resistance to the cortical plates. Once the infection penetrates the cortical plates, they reach the muscle plane.1 If the infection perforated is above the muscle attachments, it’s confined to an intraoral abscess. If the cortical plates are perforated below the muscular attachments, extraoral swelling develops. The next barrier is the periosteum which is strong and elastic in nature. Once the periosteum is breached, infections reach the soft tissue planes, the fascia. Most of the infections are confined to a particular space and the surrounding fascia. Based on the toxins produced by the microorganisms, the infection can spread to adjacent spaces and even retrograde. Common deep space infections are Ludwig's angina followed by peritonsillar, submandibular, and parotid abscesses. 2 Infratemporal and temporal space infections are rarely compared to other deep space infections. Many etiological factors form the base for the infections of deep spaces, dental caries, extraction of infected, non-infected tooth maxillary sinusitis, tonsillitis, maxillary sinus fracture, temporomandibular arthroscopy, drug-induced infections. Infections of odontogenic origin, spreading along infratemporal and temporal space are most common with maxillary molars followed by mandibular molars. We report a case of retrograde spread of buccal space infection into temporal space secondary to mandibular tooth extraction.

Bowel perforation after ventriculoperitoneal-shunt placement: case report and review of the literature

Bowel perforation by a peritoneal catheter (BPPC) is a serious complication after ventriculoperitoneal shunting, with high mortality and morbidity rates. This patient presented with scalp ulceration over the shunt valve at the retromastoid region 26 years after shunt placement. During revision, the catheter distal to the valve was divided in the clavicular region. As there was no cerebrospinal fluid drainage, we decided to remove the ventricular catheter and valve. The ulceration was debrided and primarily closed. Distal to the clavicle, the disconnected peritoneal catheter was encased in a fibrous, calcified tunnel. To avoid piecemeal resection with multiple incisions, the catheter was not retrieved. Two years later, the patient presented with an abscess and pus draining from the clavicular wound. Cultures were positive for enteric bacteria. BPPC with retrograde spread of infection was suspected, and abdominal computed tomography confirmed perforation. We removed the disconnected catheter, but the perforation site could not be detected during laparotomy. The patient was treated with intravenous antibiotics and recovered without complications. To minimize complications, abandoned catheters should be avoided. Otherwise, patients unnecessarily have a life-long risk of developing abdominal complications. In patients with abandoned catheters and severe abdominal symptoms, BPPC is an important differential diagnosis.

Varicella Zoster Virus Infection of the Nervous System

Varicella zoster virus (VZV) is a human herpesvirus that causes varicella (chickenpox), after which virus becomes latent in ganglionic neurons along the entire neuraxis. Reactivation of VZV due to a decline in the cell-mediated immune response to VZV in elderly or immunocompromised individuals causes zoster (shingles), frequently complicated by chronic pain (postherpetic neuralgia) and serious neurological disease (meningoencephalitis, myelitis and VZV vasculopathy due to retrograde spread of virus after zoster. Here, we describe clinical, laboratory and pathological features of neurological complications of VZV reactivation, including diagnostic testing to verify VZV infection of the nervous system, since all neurological complications of zoster may occur without rash. We also discuss VZV latency, primate models to study varicella pathogenesis and immunity, and immunization of elderly individuals to prevent VZV reactivation.

A new Defective Helper RNA to produce recombinant Sindbis virus that infects neurons but does not propagate

Recombinant Sindbis viruses are important tools in neuroscience because they combine rapid and high transgene expression with a capacity to carry large transgenes. Currently, two packaging systems based on the DH(26S)5’SIN and the DH-BB(tRNA;TE12) Defective Helper (DH) RNAs are available for making recombinant Sindbis virus that is neurotropic (able to infect neurons and potentially other cells). Both systems produce a fraction of viral particles that can propagate beyond the primary infected neuron. When injected into mouse brains, viruses produced using these DH RNAs label neurons at the injection site, but also elsewhere in the brain. Such ectopic labeling caused recombinant Sindbis viruses to be classified as anterograde viruses with limited retrograde spread, and can complicate the interpretation of neuroanatomical and other experiments.Here we describe a new DH RNA, DH-BB(5’SIN;TE12ORF), that can be used to produce virus that is both neurotropic and propagation-incompetent. We show in mice that DH-BB(5’SIN;TE12ORF)- packaged virus eliminates infection of cells outside the injection site. We also provide evidence that ectopically labeled cells observed in previous experiments with recombinant Sindbis virus resulted from secondary infection by propagation-competent virus, rather than from inefficient retrograde spread.Virus produced with our new packaging system retains all the advantages of previous recombinant Sindbis viruses, but minimizes the risks of confounding results with unwanted ectopic labeling. It should therefore be considered in future studies in which a neurotropic, recombinant Sindbis virus is needed.

Herpes Simplex Virus Type 1 Glycoprotein E Mediates Retrograde Spread from Epithelial Cells to Neurites

ABSTRACT In animal models of infection, glycoprotein E (gE) is required for efficient herpes simplex virus type 1 (HSV-1) spread from the inoculation site to the cell bodies of innervating neurons (retrograde direction). Retrograde spread in vivo is a multistep process, in that HSV-1 first spreads between epithelial cells at the inoculation site, then infects neurites, and finally travels by retrograde axonal transport to the neuron cell body. To better understand the role of gE in retrograde spread, we used a compartmentalized neuron culture system, in which neurons were infected in the presence or absence of epithelial cells. We found that gE-deleted HSV-1 (NS-gEnull) retained retrograde axonal transport activity when added directly to neurites, in contrast to the retrograde spread defect of this virus in animals. To better mimic the in vivo milieu, we overlaid neurites with epithelial cells prior to infection. In this modified system, virus infects epithelial cells and then spreads to neurites, revealing a 100-fold retrograde spread defect for NS-gEnull. We measured the retrograde spread defect of NS-gEnull from a variety of epithelial cell lines and found that the magnitude of the spread defect from epithelial cells to neurons correlated with epithelial cell plaque size defect, indicating that gE plays a similar role in both types of spread. Therefore, gE-mediated spread between epithelial cells and neurites likely explains the retrograde spread defect of gE-deleted HSV-1 in vivo.